No .(.V..>iL..k
Boston
Medical Library
Association,
19 BOYLSTON PLACE,
♦
By Gift oiM.U)iyA\k
RHEUMATOID ARTHRITIS
RHEUMATOID ARTHRITIS
ITS PATHOLOGY, MORBID ANATOMY,
AND
TREATMENT.
GILBERT A. BANNATYNE, M.I). Glas., M.B.C.P. Ed.
Hon. Physician to the Royal United Hospital, and to the. Tioijid
Mineral Water Hospital, Hath.
BRISTOL: JOHN WRIGHT & CO.
LONDON: SIMPKIN, MARSHALL, HAMILTON, KENT & CO. Ltd.
1896.
nrc : 7 1899
/ _ — <*o— f
•T01IV WKIOIIT AM)
PRINTERS AND PUBLISHERS, BRISTOL
PREFACE.
The writing of a treatise on Rheumatoid Arthritis
involves much labour, not only on account of the
mass of literature which has to be traced and
classified, but, also, and more especially in my
case, from the recent discovery of micro-organisms
in this disease, implying, in consequence, the
revision of all its pathology, morbid anatomy,
and treatment. Such an upheaval cannot be
accomplished in a day, and this small work is
only intended to be an introduction to further
and more perfect investigation. Many parts of
it will, probably, in the near future require
revision, but it has been my ambition to avoid,
as far as possible, making any statement
unsupported by facts or by logical deductions
therefrom. I have here utilized the discovery, of
Dr. Wohlmann and myself, of micro-organisms,
which we believe to be specific to the disease,
and the latter's life history and peculiarities,
as worked out and elucidated by Dr. Blaxall.
To them both my sincere thanks are due. In
PREFACE.
the lio'lit of our discovery I have been led
to enquire into the nature of two complaints
which have been hitherto classed as only
variations of one and the same disorder. This,
for reasons given later on, I do not consider to
be correct, and I propose to study and keep
distinct Senile Arthritis from the more general-
ized and microbic disease Rheumatoid Arthritis.
Bath, 18 96.
CONTENTS
CHAPTER 1.
TAG
INTRODUCTORY AND HISTORICAL - - - 1
Nomenclature — Evidence of its Antiquity — Landre Beau-
vais — Heberden — Haygarth — Cruveilhier — Adams — Fuller —
Charcot— Devillc— Broca — Key — Senator — Garrod — Virchow
— Hutchinson — Spender -Its Individuality— Its Frequency,
etc.
CHAPTER II.
.ETIOLOGY AND PATHOLOGY - - 12
Micro-organisms a Cause — Selective Action— Where Found
— Heredity — Sex — Age — Catarrh of the Mucous Membranes
— Emotional Causes — Atmospheric Conditions — Injury —
Rheumatism — Alkalinity of the Blood — Charcot — Pye-Smitb
— Hutchinson — Forsbrooke — Dystrophic Theory — Evidence
in its Favour — Against it — Ord's Theory — Rerlex Irritation —
Functional Depression — Toxic Conditions — Muscular Atrophy
— Insufficiency of Theories — Micro-organisms — Effect on
Nerve System — Erb — Muscular Atrophy due to Toxic Causes
— Multipolar Nerve Cells — Ferrier — Folli — Condition of the
Anterior Cornua — Muscular Selection — Vaso-motor System —
Pigmentation — Sweating — Tachycardia- Bezanron -Anaemia
— Hunter — Summary.
CHAPTER 111
PATHOLOGICAL ANATOMY AND BACTERIOLOGY - 18
Degenerative Character of Changes — Points of Origin —
How the Bacteria gain Access— Naked Eye Appearances of
Joint — Changes in Synovial Membrane — -Loose Bodies — Liga-
ments— Characters of Synovia — Changes in the Cartilages—
Cornil and Ranvier — Erosion — Proliferation — Lipping —
Changes in the Bones— Rarification — Osteo-sclerosis — Volk-
mann — Changes in the Muscles — Central Nerve Changes —
Peripheral Nerves — ■ Cardiac Changes — Kidney — Blood —
Glands — Fibrous Nodules — Heberden's Nodes — Situation and
Mode of Growth — Gout a Cause— Their Nature —Various
other Views — Bacteriology, etc.
CONTENTS.
CHAPTER IV
VARIETIES ANT) DIAGNOSIS -
Errors in Diagnosis— Acute Rheumatoid Arthritis— Osteo-
Arthritis — Charcot's Classification — Post-Rheumatic, Gonor-
rhceal, and Gouty Forms — Acute and Sub-acute Forms —
Infantile Arthritis— In Children— In Adults— Differences —
Symptoms — Appearance of Joints — Chronic Rheumatoid
Arthritis — Age — Appearances — Bony Changes — Diagnosis
between it and Nerve Diseases — Charcot's Disease — Gout —
Rheumatism, Chronic Rheumatism, etc.
CHAPTER V.
SYMPTOMS AND PROGNOSIS - 97
Premonitory Symptoms — Spender — Primary Symptoms
due to Micro-organisms — Appearances of Joints — Heat of
Skin — Arthrite Seche — Synovial Pouches — Joints first Affected
— Symmetry — Ankylosis — Deformities — Dislocations — Osteo-
phyte Out-growths — Forms of the Deformities — In Hands
and Knees — Its Causes — Difference in Acute and Chronic
Cases — Cardiac Symptoms — Endocarditis — Pericarditis —
Changes in the Glands — Secondary Symptoms — Muscular
Atrophy — Its Characters — Selective Power — Myotatic Irrita-
bility— Fever— Pulse Rate — Tachycardia — Tension — Anaemia
— Haemorrhages — Purpura — Neuritis — Its Frequency — Tro-
phic Phenomena — Skin Changes — Glossy Skin — Loss of Hair
— Atrophy— Downy- growth of Hair — Pigmentation — Sweat-
ing— Dyspepsia, — Kidney and Cardiac Troubles — Prognosis.
CHAPTER VI.
TREATMENT ------- 126
Preliminary Considerations — Antitoxinc — Causes — Diet —
Clothing — Exercise — Drugs — Creasote — Guaiacol — Guaiacol
( larbonate — Benzosol— Phenols — Naphthols — Betol — Salol —
Action of Creasote— Hudeod — Douglas Powell — Intestinal
Antiseptics — iron — Arsenic — Iodides — Salicylates — Actsea
Liacemosa — Ichthyol — Hyoscyamus — Relief of Pain — Dr.
Spender's Treatment— Guaiacol Externally — Carbolic Acid
Fomentations — Electricity — Thermal Treatment — Alkaline
and Sulphurous Waters— Bath — Buxton — Aachen — Action
of Bath Waters — Batli Treatment — Hot Air Baths — Sea
Voyages — Extension— Excision — Summary.
CONTENTS.
CHAPTER VII.
PAGE
SENILE ARTHRITIS - - - 151
Morbus Coxse Senilis — Senile Arthritis — Monarticular
Rheumatoid Arthritis — In whom seen— Symptoms — Morbid
Anatomy — Changes in the Bones — Trophic Phenomena —
Treatment.
APPENDIX - - - - 156
BIBLIOGRAPHICAL INDEX - - - - - 162
INDEX - - 166
LIST OF ILLUSTRATIONS.
PLATE I, Page 70.
Photograph of bones of hand in Rheumatoid Arthritis.
PLATE II, Page 76.
Fig. A. — Synovial fluid, stained with gentian violet x 900.
Fig. B.— Beef-broth culture, stained with carbolic fuchsine
x 900.
PLATE III, Page 89.
Fig. A. — Spindle shaped enlargement of joints with atrophy.
Fig. B.— Pulpy swelling of joints.
PLATE IV, Page 90.
Photograph showing swellings in joints, etc., and general
emaciation.
PLATE V, Page 92.
Another case — the swelling being soft and doughy ; also
atrophy of right hand.
PLATE VI, Page 97.
Fig. A. — Enlargements of the heads of bones, synovial swelling
and atrophy.
Fig. B.— Ulnar deflection in a chronic case.
PLATE VII, Page 99.
Fig. A. — Showing deflection of left hand.
Fig. B. — Showing spindle shaped swelling of phalangeal joints.
PLATE VIII, Page 106.
Fig. A. — Dislocation backwards of index finger.
Fig. B. — Ulnar deflection.
PLATE IX, Page 119.
Fig. A. — Fusiform deformity of index finger.
Fig. B. — Haemorrhage under nails.
LIST OF ILLUSTRATIONS.
WOOD ENGRAVINGS.
Fig. 1. — Section through phalangeal joint in chronic Rheu-
matoid Arthritis- - - - - - 51
Fig. 2. — Osteophytes, eburnated bone, grooves on articu-
lating surfaces ------- 52
Fig. 3.— Connective tissue, showing micro-organisms - 55
Fitj. 4. — Sections through diseased cartilage - - - 59
Fig. 5. — Metacarpal bone, showing osteophytes - - 61
Fig. 6. — Osteoclast eating bone ------ 63
Fig. 7. — Multipolar ganglion cells from anterior cornua 64
Fig. 8. —Portion of nerve, showing neuritis 65
Fig. 9. —Head of femur from case of morbus coxas senilis 153
CHAPTEE I.
INTRODUCTORY AND HISTORICAL.
Nomenclature — Evidence of its Antiquity — Landre Beauvais —
Heberden, — Hogarth — Cruveilhier — Adams — Fuller — Char-
cot— Deville — Broca — Key — Senator — G-arrod — Virchow—
Hutchinson- —Spender — Its Individuality — Its Frequency, etc.
HITHEKTO, the disease which we call Kheumatoid
Arthritis has not only been known by different
names, but different diseases have been classed
under this heading— the number and diversity of the
terms employed corresponding in a certain sense with
the number and diversity of the views advanced with re-
gard to its aetiology and pathology. It is undoubtedly a
disease per se, and has probably existed as such as far
back as any other known form of disease, but it was not
until the beginning of this century, or the end of the
last, that it came to be recognised and differentiated from
the allied disorders, gout and rheumatism. Indeed, I am
not certain, that in some countries it is even yet recog-
nised as a separate form of disease, for in France some
still hold it to be only a form of chronic rheumatism.
This is curious, as one of the best works ever written on
the subject was penned by that great observer, Charcot.
Much of the difficulty surrounding the disorder is, I am
sure, caused by the ambiguity of the various terms which
have, at one time or another, been applied to it, and none
of which seem exactly to describe its characteristics, but
leave much to the imagination of the individual observer.
Of recent years the principal terms employed to desig-
nate it have been those of rheumatoid arthritis, and osteo-
1
2 RHEUMATOID ARTHRITIS.
arthritis. Now how much better would it be were we
content with one name only, even if that one did not
actually describe the condition with perfect accuracy ?
What an amount of confusion might have been saved !
This want of exactitude in nomenclature would soon
have been compensated for in our increased knowledge,
which we would have been enabled to store up and note
for comparison about a complaint, the study of which,
and the disentanglement of whose literature and prevail-
ing impressions, are enough to appal even the boldest.
Many and various are the theories which, at one time or
another, have been advanced to explain the congeries of
symptoms called rheumatoid arthritis ; and many and
various are the diseases, which, at one time or another,
have come under our notice labelled rheumatoid arthritis,
osteo-arthritis, rheumatic gout, etc., these terms being,
as a rule, quite indiscriminately apportioned. No wonder
confusion has reigned supreme. As far as our still
limited knowledge renders possible, I will endeavour to
throw a ray of light into the obscurity surrounding the
aetiology and pathology of the disease, with the hope
that it will, in the near future, enable us to walk with
surer footsteps.
Of the many names used to designale the acute or
destructive form of the disorder, I have here assumed
that that of rheumatoid arthritis is the one best known to
the largest number, and, therefore, the one best suited
to be used permanently. It, in my opinion, is the one
fulfilling to the greatest extent the requirements of
science. This term was first applied by Garrod, and
although it implies a condition which many deny exists,
yet I think, from every point of view, it is the most suit-
able. It has been objected that the word Eheumatoid,
which means, freely translated, like rheumatism, is mis-
leading ; so it is, to a certain extent. Yet no one
INTRODUCTORY AND HISTORICAL. 3
will deny that while quite separate and distinct, it, to a
certain extent, in outward appearance at least, does
resemble some forms of rheumatism. It is a much
more suitable term than any of those which include
Eheumatic, as part and parcel of their being. Bheu-
matic applies to a totally different condition, and to bring
it in leads to endless confusion . Osteo-arthritis is a term
implying a condition much more marked in the chronic
forms of the disease, and which I would keep for those
chronic osteo-sclerotic cases, so often seen in the later
stages. Some have objected to the use of arthritis at all,
as they hold that the inflammatory changes in the joints
are merely secondary to nutritional changes elsewhere ;
were it not for this, the term most commonly used in
Germany, arthritis deformans, would have become much
more popular. This objection to arthritis can hardly be
sustained, especially in consequence of our newer light
on the origin of the disease.
The following is a list of the terms which have, at one
time or another, been applied to the disease : —
1. " Goutte Asthenique Primitif," by Landre Beau-
vais, in 1800.1
2. " Digitorum Nodi," by Heberden, in 1804.2
3. " Nodosity of the Joints," byHaygarth, in 1805.3
4. " Chronic Eheumatism of the Joints," by Todd, in
1843.4
5. "Arthrite Seche," by Deville and Broca, in 1848
and 1850.5and6
6. " Eheumatic Gout," by Fuller, in 1852.7
7. " Eheumatisme Chronique Primitif," by Charcot
and Vidal, in 1853 and 1855.8
8. " Usure des Cartilages Articulaire," by Cruveilhier,
in 1858.9
9. " Chronic Eheumatic Arthritis," by Adams, in
1857.10
4 RHEUMATOID ARTHRITIS.
10. "Kheumatisme Noueux," by Trousseau, in I860.11
11. " Arthritis Deformans," by Virchow, in 1869.12
12. " Eheumatoid Arthritis," by Garrod (Sir A.), in
1876.1::
13. " Osteo-arthritis," by Spender, in 1888. 14
14. " Pernicious Arthritis," by Brabazon, in 1896.66
From this list we see, that even from the beginning,
there has been a difference of opinion as to what is, and
what is not rheumatoid arthritis, as well as an uncer-
tainty as to the nature of the morbid process ; some
ascribing the changes to rheumatism, whereas others have
thought they were gouty in nature ; some, in their
writings, describing typically rheumatoid cases, and
others as typically what are not rheumatoid.
Turning to the history of this complaint, we find its
characteristic changes (probably osteophytic) have been
found in the bones of its victims in times which, if not
quite prehistoric, are practically so. As far as I can
learn, the oldest bones showing these changes are those
found in lower Egypt by Mr. Petrie,15 who suggests as a
probable, date 1300 B.C. Next come those discovered by
Mr. Eve,1G also in Eg}rpt, and probably referable to the
Ptolemaic period (second century B.C.) ; and following
on these are those of a Norse Viking, found in the
Christiania Fjord; those found in Pompeii, by Chiaje;17
those in the Convent of Marienthon in Pomerania, by
Virchow ;1S those in the Boman Sarcophagus at Smith-
field, by Dr. Norman Moore ;19 those in the Catacombs of
Paris, found by Leber t ;20 all showing distinct traces of
bony rheumatoid, or osteo-arthritic change. Coming
down to more recent times, we find the disease was first
described by Sydenham,21 from a clinical point of view,
in the year 1683, as a modification of rheumatism. In
1703 it is referred to in the writings of Musgrave ;22 in
1764 and 1768 in those of Haller 23 and De Salivates,24
INTRODUCTORY AND HISTORICAL. 5
respectively. In those writings one can trace references
to the disease, but it was not actually described as a
disease per se until the year 1800, when Landre Beau-
vais 25 published his Thesis on " G-outte Asthenique
Primitif," which condition we now recognise as one of
rheumatoid arthritis. Amongst the other features to
which he drew attention was the special liability of
women to its attacks, its chronic nature, its destruction
of the cartilage, and its enlargement and deformity of the
affected joints. He recognised that it could not be due
to gout, thus differentiating for the first time between
that disease and rheumatoid arthritis. His picture is a
typical one. In 1804 Beauvais' opinion received the
support of Heberden,26 who, however, went further, and
differentiated between it and rheumatism. He men-
tioned that there was little or no fever, no redness of the
skin, no great pain, but swelling of the affected part; that
the disease was not particularly apt to begin in the foot,
but if so, it soon ieft it and attacked other parts of the
limbs, several of which, one after the other, became the
seat of the distemper from the first fit ; that it was very
crippling ; and that one attack caused more weakness of
the limbs than would have been produced by gout in
many years. He mentions that the wrists, and some-
times the fingers were specially liable, and that often it
remained permanently in these joints. He also described
what have ever since been known as Heberden's nodes,
as occurring on the terminal phalanges of the fingers.
In 1805 Haygarth 27 published his clinical "History
of Diseases," which gives the clinical appearance of
rheumatoid arthritis, describing it fully, and also differ-
entiating between it and rheumatism. In 1813 Chomel28
alludes to Landre Beauvais' thesis, but believed that the
disease referred to by the latter was of a rheumatic type.
In 1827 Scudamore20 mentions that he had seldom seen
6 RHEUMATOID ARTHRITIS.
such cases as are described by Haygartli, except second-
ary to gout and rheumatism. In 1833 Brodie,30 in his
work on " Diseases of the Joints," calls attention to its
being quite distinct from both rheumatism and gout ;
and during the years 1829 to 1840 Ouveilhier31 wrote
mentioning the necessity of observing its clinical charac-
teristics, and gave it the name, " Usure des cartilages
articulaire." He points out that true bony ankylosis
may occur. During this period also it was studied and
commented upon by Lobstein s2 (1833), Key33 (1833),
Eobert Smith34 (1835), Canton35 (1848), Deville 36 (1848),
Broca 37 (1850), and Adams 38 (1857) in this country and
France ; whilst in Germany, Meyer 39 (1849\ Weber 40
(1858), and Leis 4] wrote explaining the rationale of the
various phenomena observed. These were subsequently
confirmed by Cornil 42, Vergely43 (1858), and Banvier 44
(1865). Broca and Deville gave it the name " Arthrite
Seche," and Adams that of " Chronic Bheumatic
Arthritis." Eobert Smith and Adams both pointed out
that many cases of disease of the hip joint, resulting
from injury, were of the nature of rheumatoid arthritis,
and thereby caused confusion with regard to malum
eoxae senile. Adams gives many beautiful illustrations
of the morbid anatomy. He says Sandifort,45 of Leyden,
was the first to notice the disease, in the hip joint, in the
post mortem room. Adams also corroborates Cruveil-
hier's observation about the occurrence of true bony
ankylosis, and he mentions that the polyarticular cases
are usually preceded by acute rheumatism. Moreover,
he draws attention to the relationship between the mon-
articular cases and injury. Colles, in 1839 — 1857,
remarks that two different processes were at work, one
absorbing, and one forming fresh bone. In 1843 Todd 4(5
called it " chronic rheumatism of the joints," and con-
sidered the changes to be more of an irritative than in-
INTRODUCTORY AND HISTORICAL. 7
flammatory nature. In 1849 Kedfern 47 gives some
good illustrations of the disease, and shows the nature of
the cartilaginous changes. In 1852 Fuller,48 in his
work on " Eheumatism and Allied Disorders," calls it
" rheumatic gout." He says that although it is in some
respects closely allied to rheumatism, yet he considers it
more of the nature of gout ; at the same time he
thinks it is not a compound of the two disorders, hut a
distinct disease. In 1853 Charcot and Trastour49 pub-
lished their thesis. As Charcot's views have been more
largely received and criticised than any other, his
opinions will come under consideration later on, and as
they crop up. In 1855 Vidal 65 followed Charcot with his
thesis. They all three give it the name " Kheumatisme
Chronique Primitif," and they all held that it was only
a form of chronic rheumatism. This view is still held in
France by many, as may be seen from Charcot's later
writings, and also from those of Besnier,50 Homolle,51
Lacaze-Dori,52 and Mathieu.53 In England, America,
and Germany, this is not the view held by most writers
on the subject. Most of them have been of the opinion
that Heberden and Hay garth were right in regarding it
as a disease per se, and that although it presented many
outward appearances, resembling both gout and rheuma-
tism, yet it differed entirely in essentials, and that it was
evidently a distinct disorder. Adams and Fuller, who
did much work in the elucidation of the characteristics
of the disease, held this view, and coming down to more
recent times we find that Sir A. Garrod54 showed unmis-
takably that the excess of uric acid, present in gout, was
entirely absent in rheumatoid arthritis. It was classed
by him under three headings, namely, acute, chronic,
and irregular. The chronic form he further subdivided
into general and local. Since then many have written
on the subject, and their studies have brought about a
8 RHEUMATOID ARTHRITIS.
profound change in the prevailing views as to its nature.
Senator 55 describes it under the name of " Arthritis
deformans," which had previously been given to it by
Virchow,56 and he believed that it was a true constitu-
tional disease. Hutchinson 57 looked on it as the result
of a rheumatic diathesis, caused by the blending of the
elements of gout and rheumatism, now the one and
now the other element predominating. In 1884 Sir
Dyce Duckworth58 gave it the name of " Chronic rheu-
matic arthritis," and thought it was a form of true
rheumatism. Lane59 (A.), in 1884, thought that the
changes in the joints were caused simply by wear and
tear; and Ord,60 in 1885, considered it to be purely of
reflex nervous origin. Spender,61 in 1888, pointed out
some of the early nerve phenomena under the name of
osteo- arthritis. In 1890 Dr. A. E. Garrod62 calling it
" Rheumatoid arthritis" wrote a treatise on the
subject ; also in that year Lane (H.) and Griffiths 63
pointed out the differences between rheumatoid arthritis,
chronic rheumatic arthritis, and osteo-arthritis ; while
in 1893 Forsbrooke 64 brought out his dissertation, and
advanced the view that it was anaemia to which it and
all the vaso-motor and trophic changes were due ; the
joint changes he considered being due to trophic mal-
nutrition ; and quite recently Dr. Brabazon66 suggested
that it might be called "Pernicious anaemia," having
reference more especially to the symptoms.
Such are the main points in the history of the disease,
and one wonders that with such a mass of literature,
having direct bearing on the subject, that we should
have been so long in the dark, both with regard to its
pathology and its aetiology, and, I am sorry to say, also
with regard to its morbid anatomy. Yet such is the
case. If it is granted that we are dealing with a disease
by itself, one would look for some salient symptom or
INTRODUCTORY AND HISTORICAL. 9
symptoms, without which we would have no rheumatoid
arthritis. This we find in the joints and nervous sys-
tem. The joint symptoms are always the primary ones,
the nerve phenomena being purely secondary, but their
presence, in one shape or another, is so persistent that
one can only regard them as essential elements of the
disorder. The conjunction of symptoms is such as we
find in no other morbid process. It is not merely
occasional joint troubles, associated with nerve lesions,
or vice versa, but it is a constant conjunction of certain
symptoms, in a well marked sequence, referable on the
one hand to the joints, and on the other to the nervous
system.
Turning to the frequency with which it is met, I may
say, that it is a common form of disease occurring, as
one observer states (Haygarth), as often as 1 in every
310 patients, giving a percentage of 0*32. During the
years 1893 and 1894 there were admitted 2,405 patients,
of whom 432 suffered from rheumatoid arthritis, 1,558
from rheumatism, and 255 from gout, to the Bath
Eoyal Mineral Water Hospital. It is more common in
the poor and badly nourished, and is also more common
in the cold damp parts of the globe than in either the
dry cold or hot damp.
REFERENCES.
1. Landre Beauvais. — " Goutte Asthenique Primitif," 1800.
2. Heberden. — " Commentaries," 18047? —
3. Haygarth. — " Clinical History of Diseases," 1805.
4. Todd. — " On Gout and Rheumatism," 1848.
5. Deville. — " Bull, de la Soc. Anatom.," xxii. and xxiii., 1848.
6. Broca. — " Bull, de la Soc. Anatom.," xxv., 1850. s
7. Fuller. — " Rheumatism, Rheumatic Gout, and Sciatica,"
1852.
8. Charcot.—" These de Paris," 1853.
9. Cruveilhier. — " Anat. Pathologique," Liv. ix.
10. Adams.—" On Rheumatic Gout," 1857, and 3rd edit. 1873.
io RHEUMATOID ARTHRITIS.
11. Trousseau. — " Cliuique Medicale." ^
12. Virchow. — " Virchow's Archiv.," xlvii., 1869. ^
13. Garrod, Sir A. — " Gout and Rheumatic Grout," 1S76.
14. Spender. — "Osteo-arthritis," 1888. v'
15. Petrie. — Museum, Royal College of Surgeons, 1891.
16. Eve.—" Brit. Med. Journal," vol. i., 1890. V
17. Chiaje. — " Arthritis Deformans from Pompeii."
18. Virchow.— Loc. cit., p. 298. V
19. Moore.—1' Path. Soc. Trans.," 1883, xxxiv., p. 226. <
20. Lebert.— " Handbuch der Pract. Med.," 1859, ii., p. 874. ^
21. Sydenham. — " Opera," Sec. vi., cap. v. ^
22. Musgrave. — " De Arthritide Symptomatica," p. 24.
23. Haller. — " Elementa Physiologica," vi., p. 9. "*<'
24. De Sauvages. — " Nosolgia Methodica," class vii., order i. %
25. Landre Beauvais. — Loc. cit.
26. Heberden. — Loc. cit., chap, xxviii. >t
27. Haygarth. — Loc. cit. ?*■»
28. Chomel — " Essai sur le Rheumatisme ; These de Paris, "^
1813.
29. Scudamore— " On Rheumatism," p. 487, 1827.
30. Brodie. — " Diseases of the Joints," 1833. yk
31. Cruveilhier. — Loc. cit. X
32. Lobstein.— " Anat. Pathologique," ii., p. 348, 1833, S
33. Key.—" Med. Chir. Trans.," 1833, xviii., p. 208:
34. Robert Smith. — "Dublin Journal Med. Sciences," 1835, vi., >--
p. 208. V
35. Canton.—'4 London Med. Gazette," N.S., 1848, vi., p. 410. J*
36. Deville.— Loc cit., 1848, xxii., p. 272, xxiii., p. 141.
37. Broca. — Loc. cit., 1850, xxv., p. 435. V
38. Adams. —Loc. cit., 1857. -
39. Meyer.—" Midler's Archiv," 1849.
4.0. Weber. — "Virchow's Archiv.," Jan. 1858, p. 74. X
41. Leis. — Quoted Charcot " Syd. Soc. Trans.," "Maladies des
Viellards," p. 139. X
42. Cornil. — " Niemeyer's Internal Pathologie," vol. ii., p. 556,
(transl.).
43. Vergely.— " These de Paris," 1858.
44. Ranvier.— " These de Paris," 1865.
45. Sandifort. — " Museum Anatomicum," 1793.
46. Todd.— Loc. cit. X
47. Redfern.— " Edin. Monthly Journal," 1849. X
48. Fuller. -Loc. cit. y_
49. Charcot & Trastour. — " These de Paris."
50. Besnier. — "Diet. Enclyclop. des Sciences Med.," 1876, p.
155.
51. Homolle. — " Diet, de Med. et Chir. Prat." : Article, "Rheu-
matisme," 1882.
52. Lacaze-Dori.— " These de Paris," 1882.
53. Mathieu.— " These de Paris," 1884.
54. Garrod, Sir A.— Loc. cit. 1862—1876.
55 Senator. — " Ziemssen's Handbuch," 1875 and 1879. V«f
INTRODUCTORY AND HISTORICAL, n
56. Virchow. — Loc. cit. ^
57. Hutchinson. — " Pedigree of Disease," 1884, p. 126. J 7) *G
58. Duckworth.—" Heath's Diet. Prac. Surg.," 1886, i., p. 293. >
59. Lane, A,—" Path. Soc. Trans.," 18S^and 1886. y-
60. Ord.— " Brit. Med. Journal," 1884, ii., p. 268, and " Trans.
Clin. Soc," 1879. *
61. Spender.—" Osteo-arthritis," 1888.
62. Garrod, A. E. — " Treatise on Rheumatism and Rheumatoid
Arthritis," 1890. *
63. Lane & Griffiths.—" The Rheumatic Diseases " (so-called),
1890. *
64. Forsbrooke. -— " Dissertation on Osteo-arthritis, ;' 1893.
65. VidaL— " These de Paris," 1855.
66. Brabazon.— "Brit. Med. Journal," vol. i., 1896, p. 7237^
12
CHAPTER II.
.ETIOLOGY AND PATHOLOGY.
Micro-organisms a Cause— Selective Action—Where Found —
Heredity — Sex — Age —Catarrh of Mucous Membranes — Emo-
tional Causes —Atmospheric Conditions — Injury — Rheumatism
— Alkalinity of the Blood — Charcot — Pye- Smith — Hutchinson
— Forsbrooke — Dystrophic Theory — Evidence in its Favour —
Against it — Orel's Theory — Reflex Irritation — Functional De-
pression— Toxic Conditions — Muscular Atrophy — Insufficiency
of Theories — Micro-organisms — Effect on Nervous System —
Erb — Muscular xAtrophy elue to Toxic Causes — Multipolar Nerve
Cells — Ferrier — Folli — Condition of the Anterior Cornua—
Muscular Selection — ♦Vaso-motor System — Pigmentation —
Sweating — Tachycardia — Bezancon — Anaemia — Hunter — Sum-
mary.
I. — ^Etiology.
From the discovery, made by Dr. Wohlmann and my-
self, no doubt remains, in my mind, that Rheumatoid
Arthritis is caused by micro-organisms, which we have
found to exist in the joint fluids and tissues, and
which we, as far as our present knowledge extends,
look upon as specific. How the micro-organisms gain
access to the system is not at present known definitely,
but they probably do so through some chronic catarrh
of the respiratory, gastro-intestinal or genito-urinary
systems. Such catarrhs are not far to seek in this
disease. In not a few cases it has been traced, almost
with certainty, to an attack of tonsillitis, and we know
how common disorders of the intestinal and generative
systems are. A catarrh of the mucous membranes acts
by producing mucous abrasions, upon which the micro-
organisms can settle ; by weakening the epithelial cells
in favour of the parasite ; and also by weakening the
AETIOLOGY AND PATHOLOGY. 13
nutrition and vital energy of the body generally. With
such conditions it is easy to see there will be little
difficulty in the micro-organisms gaining access to the
blood, and, having once obtained a footing in the circu-
lation, they will pass freely to all the organs of the body.
This accounts for the symmetry of the disease, and why
one joint after another comes to be involved. The micro-
organisms can now proceed to select a suitable nidus in
which they may grow and propagate. Like all other
pathogenic bacteria they exhibit a selective power, in their
choice of a habitat, which never varies. What governs
this selective power we know not ; but it appears curious,
that out of all the sites to which they obtain access,
they should, as far as we at present know, only choose
the joints. We know, that in relation to different
causes of disease, the various tissues of the body exer-
cise the most markedly different influences, even though
the cells constituting these various tissues have ori-
ginally sprung from the same cell. This difference is
not limited to the various tissues of the same species of
animal, for, when we compare different species, we find
that even the same organ or form of tissue may present
the most marked differences in relation to the factors
giving rise to disease. For example, we see how in man
the liver is an inhospitable host to the bacillus of
tubercle. But it is not so with the liver of the ox or
the guinea-pig. Of similar import is the fact, that if
we examine every one of the pathogenic microbes, we
will find different species of animals presenting very
varying degrees of susceptibility. Even in the case of
such a disorder as anthrax, there are all varieties
amongst the various species, from immunity in the frog,
to extreme susceptibility, as in the mouse and guinea-
pig. This variation in susceptibility applies not only to
species, but to varieties and races of animals and men.
i4 RHEUMATOID ARTHRITIS.
It is well known that the white rat presents an almost
complete immunity to anthrax, and that the Algerian
sheep are much less susceptible than other breeds. A
similar fact is observed in man in this respect, that
negroes are, as compared with white men, singularly
insusceptible to yellow fever.
Turning again to rheumatoid arthritis it may be noted
that joints are specially liable to bacterial infection,
vide such diseases as pyaemia and gonorrhoea. If, as
seems likely, acute rheumatism is due to bacteria, or
their products, we have yet further proof of this peculiar
liability. In rheumatoid arthritis, as in acute rheu-
matism, ulcerative endocarditis, etc., it is possible that
the bacteria also grow on the endocardium and peri-
cardium, as otherwise it is difficult to account for certain
symptoms. This point has not yet been fully eluci-
dated. It is probable that they grow freely in the
lesions through which they gain entrance, and possibly
also in other localities. So far we have no proof one
way or another on this point, so must leave it for
future consideration. In the joints themselves we have
positive proof that the organisms grow and propagate
freely, doing so not only in the synovial fluid and mem-
brane, but also in the ligamentous, cartilaginous, and,
to a less extent, in the bony structures. Their presence
gives rise to acute inflammatory changes leading on to
ulceration, erosion, and destruction of the hard as well
as of the soft tissues. This process varies in intensity
and, usually as the disease progresses, is accompanied
by a coincident, but varying amount of reparative
change which may end in a general hardening and
thickening of bones, cartilage and ligaments. This
change appears to occur either when the bacteria have
exhausted the pabulum on which they exist, or else it is
an attempt on the part of nature, to limit and shut off
.ETIOLOGY AND PATHOLOGY. 15
the disease. Possibly the production of toxic products
may play some part in this matter. The presence of
micro-organisms can be demonstrated in the joint fluids
by staining reagents, and also in the tissues on section.
The joint and heart symptoms (with possibly the gastro-
intestinal and genito-urinary catarrhal symptoms),
which are due to the direct action of the micro-organ-
isms themselves, may therefore be regarded as primary
or essential ; whilst those which are due to their indirect
action, by the absorption of their products may be
regarded as secondary or symptomatic. Although these
latter vary in every case, not only in intensity and in
nature, yet they would appear to have a common
toxsemic origin ; and some symptom of this toxaemia is
invariably present.
Let us now, for a moment, turn to those causes which
are likely to bring the body generally into such a con-
dition as to be susceptible to the attacks of those
parasites, for we know that, in health, the tissues are
able to resist all such inroads. As has been stated, the
disease may be primary in its onset or else secondary to
such diseases as rheumatism, gout, or other arthritic
condition. Apart from these, the causes, which predis-
pose to it, are all those which have, by some means or
other, lowered the constitutional state. Of these causes
the principal are : —
1. Heredity. — It is difficult to prove direct inheritance,
not only on account of the difficulty in the diagnosis,
but also on account of the confusion as to what the
name rheumatoid arthritis means. It may happen
likewise, even although the proper nomenclature is
understood in the individual cases, that the disease may
have passed over one or more generations. It may there-
fore be described as occurring sporadically; and that, out
of a family of brothers and sisters, some are affected, but
1 6 RHEUMATOID ARTHRITIS.
others have escaped. Heredity, therefore, is very hard
to trace. It is known besides that an inherited ten-
dency to disease does not in all cases manifest itself, in
an exact reproduction of the morbid peculiarity of the
parent, in the child ; but may tend to give rise to allied
conditions. Thus, it may happen, that in those in-
heriting an arthritic diathesis, in some rheumatoid
arthritis may develop, in others gout, and in others
rheumatism. Statistics go to prove that a certain dia-
thetic predisposition to arthritic disease does exist.
By this we mean a diathesis in general, not in special,
and in all cases it is easier to trace and to prove this
inheritance of a diathesis than of a disease itself. One
member of a family may have gout, one rheumatism,
whilst yet another rheumatoid arthritis. In the case of
gout and rheumatism heredity has been clearly proved,
and this is probably due to the fact that they are both
diseases wrell known and have been readily recognised for
ages, whereas rheumatoid arthritis has not. By some it
has been said also, to be peculiarly liable to occur in
those inheriting a tendency to phthisis. This is as one
would expect. The rheumatoid micro-organisms would,
in such cases, find a system weakened and unprepared
to resist their inroads, and which would therefore in all
probability fall an easy prey.
As a cause heredity was recognised early in the
history of the complaint, for w7e find that Heberden,1
Adams,2 and Fuller,3 amongst the early observers, all
mention it. Coming down to more recent times we find
a history of heredity was obtained in 11 out of 41 cases
by Charcot,4 and in 10 out of 45 by Trastour.5 These
statistics are quite unreliable, however, as these ob-
servers only regarded rheumatoid arthritis as one of the
forms of rheumatism, and as such the family history
was taken. GarrodG traced in 84 out of 500 a direct
^ETIOLOGY AND PATHOLOGY. 17
descent, giving a percentage of 16*8. The average per-
centage of heredity, in rheumatism (taking the results
of Fuller, Syers, Pye- Smith, Garrod, etc.), is 23*9.
When we consider the inheritance of other forms of
arthritic disease, in rheumatoid arthritis, the percentage
is much greater. Garrod 7 gives a percentage of 432.
On farther analysis he mentions that there was a history
of gout in 20 per cent., whilst only 12*8 gave one of
rheumatism. This is very remarkable, and I have quite
failed to verify it. Sir A. Garrod and Sir Dyce Duck-
worth point out that the disease is most common in
female members of gouty families. My statistics do
not carry this out, for taking one year at the Bath
Koyal Mineral Water Hospital (1894-1895), I had 78
patients suffering from rheumatoid arthritis, and of
these only 4 gave a history of direct inheritance. In
none could gout be clearly traced. In several there was
a history of rheumatism affecting a brother or sister,
and in 12 affecting a father or mother ; but never one of
gout that could be depended upon. In other years I
have obtained such histories, but they are so apparently
accidental that I have been quite unable to substantiate
this theory. The class of patients, whose statistics I
have taken of course may, to a certain extent, account
for this, but not entirely. Heredity does not seem to
render a patient more liable to be attacked in early life,
but it does seem to affect the acuteness of the disorder.
2. Sex. — There can be no doubt that the disease is
much more common in women than in men. Out of 78
cases 9 were in men, and the rest in women (11 • 5 and
88*5 per cent.). Gout affects men more commonly,
whereas rheumatism does so in nearly equal propor-
tions. Hay garth 8 found 1 man to 34 affected, and
Garrod9 found that it occurred in 411 females to 89
males (82*2 and 17*8 per cent). As was pointed out by
1 8 RHEUMATOID ARTHRITIS.
Adams, Senator, and others, the joints most affected in
men, are the larger ones, such as the hip or shoulder,
and in women, the smaller ones. Charcot, Trousseau,10
Duckworth, and others, have also observed it to be more
common in women. This frequency in women is almost
certainly due to the frequency of some genito-urinary
derangement, some abnormal condition of which is pro-
bably one of the commonest roads by which the micro-
organisms obtain access to the blood, and thence to the
joints. In the case of children it is more common in
boys than in girls — the younger the child the greater
the proportion of males. As puberty is approached this
diminishes until the proportion of females equals, and
finally greatly exceeds that of males.
3. Age. — Much has been written about the age at
which the disease most commonly commences. By
most it is held to be essentially a disease of the early
degenerative period. Many of the acutest cases occur,
however, in young adults, and often even in children.
Dr. A. E. Garrocl11 shows that the commencement of the
disease steadily increases with each five-yearly period,
until that between 45 and 50 is reached, after which the
number rapidly falls. In males, on the other hand,
the decrease does not occur until 70 has been reached,
and in them also there is no steady increase, but two
maxima exist, one between 30 and 35, and the other
between 50 and 55. The special liability of women,
between the ages of 40 and 50, is probably due to the
occurrence of the climacteric. In women there are two
great periods in life — the period of puberty, and that of
the climacteric. The former is a time of great strain, both
mentally and physically, not only on account of the new
conditions which the reproductive organs have taken on,
but also on account of the general bodily conditions
induced thereby. It is a period attended by a general
^ETIOLOGY AND PATHOLOGY.
19
aptitude for disease, as there is a special connection
between the physiological processes going on, and the
general bodily health. At the same time women are
liable for less obvious reasons to the attacks of disease
of various kinds. The period of the climacteric is at the
other end of life, answering in many respects to the
period of puberty in being a time in which the whole
system is in a state of unrest, unstable and ready to
develop unhealthy tendencies. Unfortunately it is a
degenerative process, and, from its very nature, we
would expect to find it more productive of mischief.
The sudden fall in the number of cases occurring after
the menopause is probably due to the fact, that all
uterine activity having ceased, there are fewer roads by
which the micro-organism can gain access — at least its
most common road is closed. It is almost certain that
a climacteric occurs in men in a similar fashion, but it
is not so marked, and probably occurs later in life.
The following is an analysis of 78 cases : —
AGES OF FIRST OCCURRENCE.
FEMALES.
MALES.
Between 10 and 20
„• 20 „ 80
80 „ 40
40 „ 50
50 „ 60
,, 60 ,, over
4
16
25
12
H
1
1
4
3
1
Totals
69
9
4. Catarrh of the Mueous Membranes. — How far a
catarrh of the mucous membranes of the respiratory,
gastrointestinal, or genito-urinary systems acts, as a
predisposing cause, it is hard to say ; but that it is
through its agency that the micro-organisms finally
20 RHE UMA TOW AR THRIT1S.
gain a footing is almost undoubted. I have traced
the onset of the disease in several cases, almost with
absolute certainty, to chronic catarrhal tonsillitis ;
several to the onset of dyspeptic conditions ; and a
still larger number to the onset of genito-urinary
troubles. It is a frequent follower of confinements,
and, more rarely, begins during pregnancy. Uterine
derangements are responsible for the onset of many
disorders, but none more markedly so than rheu-
matoid disease ; and how can we wonder at it,
when we find, as a consequence of some local irregu-
larity, women in a state of mental worry, anxiety,
sleeplessness, pain, and nervous exhaustion, both their
mental and physical powers being at their lowest ebb ?
I)r. Ord laid special stress upon this fact, and I think it
is well merited, though for different reasons. He
noticed that, in certain instances, the disease in the
joints was limited to one side ; and in these cases there
was ovarian pain, and tenderness on the same side as
the joint lesions. He also noticed paroxysms of pain
occurred with the monthly periods. He considers these
uterine and ovarian derangements to be the cause of
the disease, through reflex action. To my mind, it is
more probable that they only act as affording a lesion
through which they may reach the circulation ; and,
by the induced irritation and debility, render the
system so lowered and impaired as readily to fall a
victim.
In 78 cases, 1 was due to tonsillitis ; 4 occurred after
confinements ; 1 during pregnancy ; and 1 after a mis-
carriage.
In a large number there was irregularity in the
monthly functions, but I rarely could trace a case
directly to these disorders. Garrod says that 105 out of
176 were normal in their menstruation. Five occurred
.-ETIOLOGY AND PATHOLOGY. 21
soon after a confinement, 3 after miscarriages and 8
during pregnancy.
5, Emotional Causes. — The influence of these is not
confined to the period immediately preceding the onset
of the disease, but it also to a certain extent influences
the progress of the disorder. Over and over again do we
find patients who say they are worse after any anxiety
or worry. The disease has been known even to arise
after prolonged worry ; but in such cases worry probably
only acts by lowering the tone of the constitution. Other
mental causes assigned have been sudden shock and
fright. Both Kohts12 and Leyden13 mention cases in
which it occurred after severe shock, caused by the
bursting of shells in time of war.
6. Atmospheric Conditions. — Eheumatoid arthritis is
most commonly met with under those influences most
favourable to the prevalence of catarrhal and inflam-
matory affections of the air and digestive tracts, that
is, on cold and damp soils with a variable temperature,
and as we know at those seasons of the year, the spring
and autumn, when these conditions are most likely to
prevail. Professor Charcot regarded a combination of
damp and cold as the most potent cause. He was of the
opinion that the exposure, to such influences, must be
prolonged, and that articular lesions did not necessarily
arise until some time had elapsed. Many sufferers
ascribe the onset of their complaint to dampness, and
there can be no doubt that cold and damp often
markedly increase the misery of the wretched patients.
The disease is more common in Ireland than in Eng-
land, and this is accounted for by the prevalence of
damp in the former country. Adams14 has pointed out
that it is specially common in Holland. Although a
dry climate is least favourable to its development, it is
not unknown in any locality. In this respect we are apt
22 RHEUMATOID ARTHRITIS.
to confound, and it is difficult to avoid confounding, its
indirect effects as predisposing agents with its direct
effects as exciting cause. Further, when we would test
the relative influences of atmospheric conditions, our
endeavours to arrive at a just conclusion are seriously
hampered by the co- existence with them (but partly no
doubt arising out of them) of peculiarities of habit, and
modes of life, and other special conditions of unhealthi-
ness. Out of 78 cases, 2 developed after getting wet,
and 1 after a chill.
7. Injury. — Injury, as injury pure and simple, has not
a marked effect on the occurrence of acute rheumatoid
arthritis. In only a few cases have I been able to trace
a direct history of its onset to traumatic injury, but if
we look at it in its wider sense it comes to have a much
more important bearing. In the joints an injury, in its
immediate consequences, may appear so trifling as to
merit little or no attention, yet it may, in its ultimate
results, end in the crippling and loss of the use of an
important member of the body. Occasionally, but more
rarely, it appears to follow on some injury which has set
up some acute inflammatory condition. In one case I
found it occur subsequent to fracture of a patella, and
whilst the patient was in the recumbent position in con-
sequence of this fracture. A history of such direct
injury, and its consequences, is rare. One more often
hears of injury after a joint is diseased, and then the
question of effect and cause comes to be a difficult one.
If we regard injury as having a broader meaning, and look
on it as any lesion of the joint structures may-hap
caused by traumatism, may-hap by disease, then our idea
of the importance of injury as a cause alters. In 78
cases 20 occurred after acute or chronic rheumatism.
I here regard the injury caused to a joint, more
or less of the nature of a direct injury, when caused
^ETIOLOGY AND PATHOLOGY. 23
by rheumatism, gout, gonorrhoea, or any other form
of arthritis which may so frequently precede a
rheumatoid onset. That rheumatoid disease frequently
follows such attacks is not to be wondered at, when we
remember the injury done to a joint by such an attack,
and when we consider that rheumatism, and most other
forms of acute arthritis, are probably caused by micro-
organisms— at least, at present there seems to be good
ground for believing that such is the case (15 and 36).
Arguing then on analogy, we may assume that one form
of organism may predispose to the attacks of another.
What the exact mode of action in these cases is we
know not ; whether they act by reducing the resistent
power which normally exists in all tissues — but in this
case more especially in the joints, or else of the blood,
which, as is stated by, amongst others, Ewing17 and
Foder,ls occurs from anything which reduces its alkalinity
and thereby its germicidal power, we at present
know not. Ewing found that normal blood serum is a
powerful protective agent against the inroads of bacterial
infection, and that toxines act harmfully, not merely by
their direct effect, but also by lowering the resistant
power of the blood against secondary infections. He
found that snake poison, which in its nature belongs to
the same class of poisons as those formed by bacteria,
greatly lowers the blood's germicidal power. Dr. Fodor
records a number of experiments showing the influence
of the alkalinity of the blood on diseases produced by
micro-organisms. Four series of experiments on ani-
mals are first reported which show clearly that, by the
administration of alkalies (sodium bicarbonate by the
mouth or by subcutaneous injection), the power of
resistance against infection with cultures of anthrax
bacilli is greatly increased. The normal alkalinity of
the blood was determined bv the examination of seven tv-
24 RHEUMATOID ARTHRITIS.
six healthy rabbits, and four experiments are reported
showing the increase in the alkalinity of the blood which
occurs after the administration of sodium bicarbonate.
He then records the results of a large number of
observations on the alkalinity of the blood in rabbits
after infection with the bacilli of anthrax, cholera,
typhoid fever, tuberculosis, and erysipelas. These
observations show that in the living organism, after
infection with certain bacilli, there is first an increase
of the alkalinity of the blood and then a diminution of
the same, more or less. If the infection is fatal, the
diminution of the alkalinity is marked and progressive ;
if not fatal, the diminution is slight, and is followed by
an increase of the same, in consequence of which the
alkalinity of the blood becomes permanently higher than
before the infection. Thus there exists a connection
between the pathological action of certain bacteria and
the alkalinity of the blood. Those rabbits having the
greater alkalinity of the blood, as well as those in which
the alkalinity of the blood is increased to a greater
extent alter infection, have greater power of resistance
against certain infectious organisms (anthrax bacilli)
than the rabbits in which the alkalinity of the blood
is less. It appears, therefore, that the degree of
alkalinity of the blood, as well as the power of the
organism to increase this alkalinity with corresponding
intensity after infection, is of essential influence upon
immunity.
I herewith append a list of the causes assigned in 38
cases out of 78 : —
After confinement ... ... ... ... ... 4
,, miscarriage ... ... ... ... ... 1
During pregnancy ... ... ... ... .. 1
Alter acute rheumatism ... ... ... ... 20
,, chronic rheumatism ... ... .. ... 1
,, getting wet ... ... ... ... ... 2
hard work ... ... ... ... ... 3
sETIOLOGY AND PATHOLOGY. 25
After, diphtheria
,, tonsillitis ...
,, influenza ...
,, fractured patella ...
,, concussion of spine
„ necrosis of the jaw from caries of teeth
Total 38
In the other 40 instances the causes given were either
too unreliable or could not be traced.
II. — Pathology.
Turning to the views which have, from time to time,
been advanced as to its pathology, we find a variety of
theories which I will shortly state and criticise.
i.— According to Charcot, and most French observers,
it is only a secondary form of rheumatism, but as, in the
majority of cases the disease arises as a primary one,
we have no ground of this belief. It, undoubtedly, may
arise as a sequela of acute rheumatism, or in fact of any
acute arthritis; but to say it is only a form of rheumatism
is, I think, grossly misrepresenting the disease, and its
characteristics. One has only to look at its clinical
characters, quite apart from its morbid anatomy, to
perceive the difference. In this country it has always
been regarded as a disease yer se, at least ever since its
peculiarities were thoroughly appreciated, and, I think,
it is hardly neccessary, for me here, to point out each
individual difference, but will take it for granted that in
this country this individuality is admitted.
ii.— Dr. Pye Smith i9 holds that the disease is often of
a senile character. This is not often the case in true
Eheumatoid, and something more than senility must
exist, in the acute cases, as they mostly arise in the
young or comparatively young.
iii. — Hutchinson 20 looks upon it as simply a result of
the combined action of the rheumatic and gouty processes,
2 6 RHE UMA TOW A R THRU IS. '
now the one and now the other element predominating.
He believes in a basic Rheumatic diathesis, capable of
subdivision into off-shoots. In many ways such a theory
is supported by facts ; but we must regard this basic
diathesis as only a diathesis. The poison of gout is as
different from that of rheumatism as they are both from
that of rheumatoid arthritis. We are positive, however,
that a certain form of diathesis does predispose to
arthritic changes, but what these changes may be will
depend on local conditions.
iv.— Forsbrooke 21 holds that the anaemia, which is
present in this disease, is responsible for the joint and
other changes. He states that at first, owing to the
deficiency of oxygen in the blood, the vaso-motor centre
in the medulla is stimulated, and by consequent con-
strictions of the minute vessels supplying the joints and
smaller nerves, the nutrition of these parts is interfered
with. This deprivation of blood, which although at first
functional in nature, may give rise to organic change.
The stimulation of the vaso-motor centre, if prolonged,
ends in exhaustion, followed by dilatation of the joint
vessels and inflammation. Ingenious as this theory is, it
rests on the assumption that anaemia is present before
any of the joint or nerve troubles. This has not been
found to be the case, so how can it be the cause ?
Personally, although I have noticed anaemia in a large
proportion of cases, it has not been invariably present,
and it has certainly not been the first symptom. It is
more likely that the anaemia is caused by the poison
generating the disease ; and is therefore only a sequela,
not a cause. The anaemia of rheumatoid arthritis has
all the characteristics of a toxaemic anaemia, and is more
fully considered elsewhere (p. 41).
v.— Remak, 22 Senator,23 Ord,24 Sir Dyee Duckworth,25
and many others, have all been of the opinion that
sETIOLOGY AND PATHOLOGY. 27
the disease is due to some abnormal trophic condi-
tion, although they differ as to the cause being due
to a primary lesion of the nervous system or only
secondary to a lesion elsewhere. Most of them hold
that the joint changes originate in a similar manner to
those occurring in Tabes Dorsalis. But tabetic changes
are due to a degeneration of the intermedio-lateral tract,
with a corresponding degeneration of the peripheral
nerves, and, as no such degeneration has yet been found
in rheumatoid arthritis, we may probably safely assume
that this argument is erroneous. This is what is called
the Dystrophic theory. If due to trophic changes one
would look for some gross organic lesion either in the
central nervous system (a), or in the peripheral nerves (b) ;
or else some reflex (c), nutritional (d) or toxic (<?) condi-
tion might exist which could give rise to the necessary
abnormal impulses.
(a,) If clue to a gross change in the central nervous
system the lesion will, of necessity, be so extensive that
we can think of no condition, which could possibly give
rise to it, unless it be a blood one. A poison circulating
in the blood is the most likely agent to affect the exten-
sive area necessarily involved : for we must remember
that the trophic influences which govern the nutrition of
the joints, bones, and skin are under the control of the
cord, the centre being probably situated in the inter-
mediate grey matter, whilst that of the muscles is con-
trolled by the anterior grey matter (probably the motor
nerve cells). As the nerve endings have a structural
continuity with the tissues, the nutrition of the tissue
molecules depends on the nutritional condition of the
nerve and nerve centres. So far no gross organic change
has been detected in the central nervous system, except
in three cases in which Folli 45 discovered an atrophic
condition in the cells of the anterior cornua. Klippel, 36
28 RHEUMATOID ARTHRITIS.
according to Massolongo, observed somewhat similar
changes, and in one case I have also observed alterations
in the conditions of the ganglion cells. These conditions
are, however, so altogether inextensive, and have been
entirely confined to the motor ganglion cells, that one
must reject the idea that they can originate such a wide-
spread disorder.
Quite apart from the question of finding gross lesions
the question is, can trophic abnormal impulses produce
such lesions as we find in the deseased joints ? I hold
that they cannot. They can, and undoubtedly do, pro-
duce muscle, integumentary, and other nutritional
changes. But can they bring about such joint alterations?
In tabes the joint changes are altogether different in
nature and appearance, and depend on a definite lesion.
In syringo-myelia they are also different. In ataxic
paraplegia, and many other forms of nerve disease, we
also see arthritic changes, but, on the one hand, they are
all accompanied by definite nerve lesions, and on the
other they seldom present more than swelling, and
effusion into the joint. A wasting, with some slight re-
parative change, one might possibly get ; but it appears
to me inconceivable that such extensive inflammatory
lesions could arise without some sure and certain guide
to a lesion, easily recognisable on both macro- and
microscopic examination. Marie,52 and 53 one of our most
accurate observers, on this subject says that the patho-
logical anatomy of tabes and rheumatoid arthritis is
quite distinct, and that although points of difference
might be mentioned, in his eyes, this is not necessary.
(b, ) If due to a gross lesion in the nerves themselves
we would expect to find symptoms of nerve degeneration,
in all and every case of rheumatoid disease — but this is
not the case. In only a certain number is an unmis-
takable neuritis present, and this so often markedly
^ETIOLOGY AND PATHOLOGY. 29
follows the arthritis that there can be no doubt it is
secondary in its nature. This neuritis may be caused by
the existing joint inflammatory process, or else it may
be due to the action of toxines circulating in the blood.
It is undoubted that toxines may thus give rise to such
a condition, thereby showing not only a -selective action
in the parts acted on, but also a peculiarity in the acting
virus. MM. Pitres and Yaillard 26 have found well-
marked neuritis in several cases, and they believe that
there is a distinct relationship between the presence of
this neuritis and the development of the trophic changes.
It must be noted that although finding marked changes
in the nerves supplying the wasted muscles yet they
found none in those supplying the articulations. On the
other hand Duplay and Cazin 27 found an inflammatory
condition of the nerves supplying the affected joints. As
will be seen, the results of such examinations have
hitherto been so uncertain and contradictory that one
must assume there is no constant occurrence of
neuritis. This agrees well with all clinical experience,
and with what one would expect from the nature of the
disease.
(c,) Dr. Orel's 2S view of the disease is that it is entirely
caused by reflex action set up by some uterine or other
visceral derangement. Although admitting that the
reflex influences, from the joints, may cause trophic
changes in the skin and muscles, and apart from the
fact that the disease occurs in men free from genital
irritation in a proportion of one to eight women, one can-
not believe that acute organic changes in the joints can
be set up by such reflex action. Trophic lesions have
been traced to injuries of the nerve centres, and of the
nerves leading to the part, but not to reflex irritation,
and there is no evidence that reflex irritation can give
rise to such lesions of the nerves or nerve centres. Dr.
30 RHEUMATOID ARTHRITIS.
Orel believes that the irritation engendered in the uterus
causes impulses to be conveyed to the central nervous
system, which in turn give rise to other morbid impulses
which are conveyed, by the peripheral nerves, to the
joints, etc., and there cause the changes which we know
by the name of rheumatoid arthritis. Although denying
that they can cause organic mischief, yet I admit, that
by causing debility and anaemia, they may so lessen the
natural defences of the joints that these may readily
become the prey of the poison, which causes rheumatoid
disease. They must therefore be borne in mind as potent
predisposing causes.
(d,) Is this disease then, as we cannot explain it other-
wise, due to a functional depression of certain areas of
the cord or of some of the peripheral nerves ? It is pos-
sible to conceive that deficient nutrition of certain areas
might set up trophic changes, and as this condition is
likely to occur in all debilitating states we would look for
it as a sequela of acute illness, or else in those who are
congenitally weak. Dr. Garrod 29 states that out of 500
cases of rheumatoid arthritis he traced a family history
of arthritic trouble in 216. Eheumatoid disease prac-
tically only occurs in debilitated people, and is often a
sequela of some acute condition which has left impair-
ment or enfeeblement of the nutritional state, both of
the body generally and of the nervous system locally.
This, however, may be said of any disease, and is only
therefore of negative value ; what is of more importance is
the fact that it would be against all experience to find
permanent symptoms, such as are seen in this disease,
arise without some slight change in the ultimate nerve
elements, which might be recognisable on microscopic
examination. If due to nutritional changes we would
look for some alteration in the medulla as being that
portion of the motor path winch has the least nutritional
AETIOLOGY AND PATHOLOGY. 31
stability. Could we explain the joint symptoms by
other means, we might readily conceive how nutritional
changes might be set up which would account for the
trophic and vaso-motor symptoms. In this probably
lies the truth.
(e,) With regard to the toxic action of bacterial poisons
on the nervous system it is of importance to note that
nutritional, as well as actual organic changes, may result.
The nerves under these circumstances are usually more
liable to be affected than the spinal cord. Toxic agents,
however, often exhibit a remarkable selective action, and
as yet we do not know what are the influences which de-
termine such susceptibility. For example, take the case
of alcohol, which being itself the result of the growth of
organisms, and being almost as low in the scale as the
bacterial toxic agents, gives rise to many and diverse
nerve conditions. To admit the action of toxic poisons
on the nerve system and exclude that of their originators
on the local joint structures would be illogical.
Having thus disposed of the more common views, let
us now consider some other arguments which have, from
time to time, been advanced to prove that the disease is
due to a nerve disorder. Thus we find Dr. Garrod 30
quoting several cases where it developed after a shock
to the nerve system. Again, Dr. Spender 31 mentions
various nerve phenomena which he has noticed occurring
at the same time, if not previous to the joint lesions. He
mentions such symptoms as pigmentation of the skin,
local sweatings, neuralgia, tachycardia, etc. He also
mentions cases where " bulbar warnings " were noticed
quite early in the disease, 3l and 32 and which progressed
to only terminate with the death of the patient. He
maintains that the arthritis does not cause the atrophy,
and that what is called " arthritic muscular atrophy,"
has nothing to do with that of rheumatoid arthritis. He
32 RHEUMATOID ARTHRITIS.
says the muscular atrophy of rheumatic arthritis is a
reflex tropho-neurosis, a pure irritation of the articular
nerves, causing atrophy through the anterior cornua of
the cord. The most difficult point to explain in rheuma-
toid arthritis is this muscular atrophy. It is one of the
most important and earliest symptoms, and is usually,
from the very first well marked. It extends to the whole
of a muscle, and not only to that part which is in contact
with the joint, or distal to it ; and it follows so closely on
the first appearance of the joint- trouble as to preclude
the possibility of extension of inflammation to the nerves.
It is found that the extensors are principally affected,
but not exclusively so. The selective character of the
atrophy is a sufficient proof that the changes in the
muscles cannot be set down to mere disease. It has
usually been attributed to some reflex nerve influence
having its origin in the peripheral nerves of the affected
joints. This has been suggested by Paget, Vulpian, 33
Charcot, and others. They argue that, assuming a
derangement of the nutrition of the motor cells of the
cord determined by the morbid impulses from the joint-
nerves, the influences from the motor cells will, in all
probability, determine the alterations in the muscle
nutrition. This theory, they hold, is supported by the
fact that by the previous division of the posterior spinal
roots, 34 and 35 wasting of the muscles can be prevented in
arthritis of the knee-joint artificially produced. Such an
argument cannot be admitted to apply to the atrophy of
rheumatoid arthritis, as this is a bacterial disease and
the experimental arthritis was not. It is known that
disease in a joint may set up spinal trouble,36 e.g.,
primary spastic paraplegia, and from this we gather that
the influences from the joint nerves act on the controlling
structure of the muscle reflex centre. The muscle reflex
centres seem also to be under the influence of other
ETIOLOGY AND PATHOLOGY. 33
centres, because if there be disease higher up they also
pass into a condition of increased activity. The path
which determines their activity is the pyramidal tract.
Other theories are that the atrophy is caused by reflex
vaso-motor spasm : this view was advanced by Brown-
Sequard; whilst Striimpell37 suggested that this inflam-
mation might have spread from the joints to the muscles,
setting up a myositis ; and in one class of cases it has
been noted by Sabourin 3S that inflammation does
spread from a joint and, affecting the nerves as well as
the muscles, gives rise to an ascending neuritis. If
neuritis has occurred the muscle fibres will be found to be
narrowed, and the shorter muscles to have undergone
proliferation.39 Vallat 40 noticed such a change in the
muscle fibres, but he found that the motor nerves were
normal. These changes were all microscopical.
We are now face to face with a difficulty. We must
either admit that the disease is one depending entirely
on an abnormal nerve condition, or else we must formu-
late a new theory as to its causation. The nerve theory
is quite unsatisfactory and unsatisfying. It explains in
a sort of way many of the symptoms, more especially
the skin changes, and muscular atrophy ; but it leaves
alone, except for a half-hearted sort of attempt, the joint
condition. Owing to our want of knowledge, as to the
morbid processes which govern the vaso-motor, and
trophic impulses, we have been unable hitherto to closely
criticise any theory advanced with regard to their method
arid mode of action, especially in cases where only some
abnormal disturbance of their functional activity exists.
Without the joint lesions we should have no rheumatoid
arthritis, and therefore unless a theory can explain this
fact we have no right to consider it perfect. It has been
mentioned already that many observers hold the changes
to be similar to those which occur in tabes ; but are they?
3
34 RHEUMATOID ARTHRITIS.
To me they appear not to be so — they differ in appearance,
in minute anatomy, and also in clinical history. In tabes
the joint changes are due to a descending degeneration
of the nerves, a change always found when looked for,
and therefore they differ in origin essentially from those
of rheumatoid disease. To my mind this fact invalidates
the whole argument.
*Turning then to the Pathology of the disease, as I un-
derstand it, and have already stated, we have a disease
due to the presence of micro-organisms found in the
joint fluids and tissues, and which must, until disproved,
be regarded as specific. How these micro-organisms
gain access to the blood is not definitely known,
but they probably do so through some chronic catarrh
of the gastro-intestinal or genito- urinary systems, and
such catarrhs are usually close at hand. In not a few
cases, as I have already mentioned, it has been traced,
with almost absolute certainty, to the tonsils. Having
gained a footing in the circulation, the micro-organisms
pass freely to all the organs of the body — thus explaining
the symmetry of the disorder, and why one joint after
another should be involved. They now proceed to select
a suitable nidus for their growth, and, like all other
pathogenic bacteria, they exercise a selective power in
their choice which never varies. What governs this
selective action is not known, but it appears curious that
out of all the sites to which they gain access they should,
as far as we at present know, only choose the joints for
their habitat. I may again note that joint tissues seem
specially liable to bacterial infection, vide such diseases
as pyaemia and gonorrhoea. It is possible that the endo-
cardium and pericardium are also liable to their attacks,
as otherwise it is difficult to account for the symptoms
referable to those tissues. Probably also the micro-
* This portion appeared in the Lancet, April 25th, 1896.
^ETIOLOGY AND PATHOLOGY. 35
organisms grow, and propagate, in the lesions through
which they gain access to the circulation, giving rise to
those local catarrhs so common during the course of the
disease. Owing to the want of post-mortem material, these
points must be left for future consideration. In the joints,
Dr. Wohlmann and I found positive proof that the micro-
organisms grow, and propagate, doing so not only in the
synovial membranes, ligaments, etc., but also in the bone-
marrow, and cartilaginous structures. Their presence gives
rise to acute inflammatory changes leading to ulcerations,
erosion, and destruction of the hard, as well as of soft
joint tissues. This process varies in intensity, and
usually as the disease progresses a co-incident, but
varying amount of reparative change is seen, which ends
in general hardening and thickening of both bones and
ligaments. The presence of micro-organisms can be
demonstrated in the joint fluids by staining, and in the
tissues on section. The joint and heart symptoms are
those only which would appear to be due to the direct
action of the micro-organisms, and may therefore be
regarded as primary or essential ; whilst those which are due
to their indirect action through their products, (definite
chemical substances produced by all bacteria), may be
regarded as secondary or symptomatic. These latter may
vary in every case not only in intensity, but in nature; yet
they would all appear to have a common origin in toxic action.
During their life cycle these, like all other bacteria,
give rise to poisonous products which being absorbed
pass to the body generally, and what is of more im-
portance, to the nervous system locally. Here again
we see either a peculiar selective action on the part of
the products acting on, or else a peculiar susceptibility
of the parts acted on. In this, as in other bacterial
diseases, we have no definite proof that it is not the micro-
roganisms themselves which cause the changes in the
36 RHEUMATOID ARTHRITIS.
nerve system, but all argument, analogy, and proof are
against their doing so ; and, therefore, I may assume that
such is the case in this disease. As evidence, we have the
experiments of MM. Vidal and Bezanc^on 41 which show
that several micro-organisms have the power of producing
central nerve degeneration, and although they have been
isolated from the blood, yet they have not been found in
the central nerve tissues. They therefore appear to act
by the elaboration of a soluble poison. Such would
appear to be the case in rheumatoid disease. With regard
to the toxic action of bacterial poisons on the nervous
system, it is of importance to note that nutritional as
well as actual organic changes may result. Although
these nutritional changes are more common in the
peripheral nerves, yet toxic agents exhibit such a re-
markable selective action, and as we do not, as yet,
know what are the influences which determine such
susceptibility, it would not be surprising to find similar
changes in the central nerve system. From every side
evidence is gathering that what may at first be only a
depression of the function of a certain centre or group of
centres may end, if the irritation be severe, whether it
be applied locally in the shape of a toxine or reflexly, in
becoming an organic degeneration, not only of that
centre or group of centres, but also of the nerve path or
paths descending from them. Erb 4'2 speaking of pro-
gressive muscular dystrophy, says there is a possibility
that the disease starting in a functional disturbance
might in the long run become associated with a coarse
lesion of the spinal centres. He says there are many
things about such a condition which agree well with this
supposition. From this we may conclude that bacterial
poisons act on either the peripheral or central nerve
system, producing, in the one case, an organic lesion, and
in another, only a functional depression.
.■ETIOLOGY AND PATHOLOGY. 37
Having accounted for the joint- symptoms by the action
of the micro-organisms, let us look at the rheumatoid
symptoms due to absorption of their products and action
on the nerve tissues. The principal, and most difficult
symptom to explain, is undoubtedly the muscular atrophy
which occurs not only early in the disease, but is one of
the most constant symptoms. The atrophy extends to
the whole of a muscle, and not only to the part which is
in contact with the joint or distal to it, and it follows so
closely on the first appearance of the joint troubles as to
preclude the possibility of an extension of the inflamma-
tion from the joint to the nerves or muscles. Apart from
true rheumatoidal atrophy we have atrophy occurring as
a consequence of a neuritis distinctly secondary in
character, and only seen in the later stages. Such a
condition has been described by Sabourin, 38 Vallat, 40
Striimpell, 37 Duplay and Cazin,27 and is of less interest
than the true rheumatoidal atrophy, and can be easily
distinguished from it as it presents all the characters of
ordinary muscular atrophy in the re-action of degenera-
tion and alteration in the muscle structure, etc. This is
absent in the true form in which the extensors are prin-
cipally, but not exclusively affected. The selective
character of the atrophy is sufficient proof that the
changes cannot be set down to mere disease. How then
do we account for it ? I think that it is due to an abnormal
condition of the multipolar nerve cells in the anterior
cornua.* It is reasonable to suppose that given a soluble
* The path of motor innervation is composed of two portions,
(a) the pyramidal cell with its dendritic processes, and centri-
fugal or axis cylinder process which courses along the pyramidal
tract, and ( bj the spinal multipolar cell with its processes, and axis
cylinder process ending in the muscle fibre. It has been shown
by Golgi's43 method of staining that the pyramidal axis cylinder
ends in an arborescence which merely comes into contact with
the spinal cell or interlaces with its dendritic processes, and
there is no actual continuity.
38 RHEUMATOID ARTHRITIS.
poison circulating in the blood, some areas in the central
nerve system should be affected, and these all the more
especially as they are in all probablity predisposed to it
by reflex irritation from the joints. That such an irrita-
tion does occur has been stated by many observers, and
has been even said to be sufficient to cause the atrophy
itself (Paget, Vulpian, 33 Charcot, and others). It has
been argued that, assuming a derangement of the motor
cells of the cord determined by the morbid impulses from
the joint nerves, the influences from the motor cells will,
in all probability, determine the alterations in the muscle
nutrition. In the light of the discovery of the micro-
organisms, and of recent observations with regard to
the action of toxines on the nerve system, we may
disregard this reflex irritation except in so far as only to
regard it as a predisposing cause. On turning again to
the cells themselves, we find according to Ferrier 44 that
the cell body with its nucleus is primarily concerned in
the nutrition of the motor nerve, and its correlated
muscular fibre, while the dendritic processes serve to
convey incitations to functional activity. He also states
that lesions of these processes may cause paralysis with all
the symptoms of a spinal paralysis, but with no muscular
degeneration. If such a condition can exist, might we
not consider it possible that by the action of a toxic body,
the cell's action might by itself be so lowered or held in
abeyance that nutritional changes in the muscles would
ensue without much disturbance of the conductive faculty
of the processes, and also without any degeneration of
the muscle beyond wasting. In progressive muscular
atrophy we have a slowly progressive lesion of the
ganglion cells, and their prolongation in the axis cylin-
ders of the nerve fibres. Might we not have on a modified
scale such symptoms if, instead of a complete destruction
of these cells, we had only a depression of their function?
ETIOLOGY AND PATHOLOGY. 39
In fact such a condition must exist, as we cannot other-
wise account for the atrophy either by reflex or direct
toxic action. The cell's vitality must be lowered. In
one class of cases, of which those mentioned by Dr.
Spender 46 may be taken as typical examples, we must
assume that the action on the cells has been so great as
actually to give rise to a distinct lesion, and this spread-
ing upwards in the pyramidal tract, has finally come to
affect the bulbar neuclei. Folli's 45 discovery of atrophy
of the motor cells, goes a long way to confirm this theory.
What was probably only at first a depression of function
due to the vascular changes set up by the rheumatoid
toxine had apparently, in the long run, become actual
organic change.
With regard to the selective site of the muscular
atrophy, we find Dr. Ferrier 47 saying, "It is not unreason-
able to suppose that the degree of representation, and
therefore the trophic strength, of the extensors in the
anterior cornua is less than that of the flexors, while
such extensors as have the most numerous connections
with the spinal segments would have a greater vital
resistance than those whose segments are fewest." From
this we may deduct that those muscles with the lowest
trophic representation will be those which are first, and
most affected, in any disease which lowers the vitality of
the nerves and nerve centres. Duplay and Cazin 4S
have suggested that it is due to the anatomical rela-
tionship between the nerves which supply the joint
corpuscles, and those which supply the affected muscles.
This does not explain it all however, and Dr. Ferrier's
explanation seems the more probable, and the more
easily understood, especially if we add that reflex im-
pulses may possibly help in the selection.
It has been proved that certain toxines have the power
of producing changes in the vaso-motor system, and also
40 RHEUMATOID ARTHRITIS.
in the trophic condition of the skin. It is thus that we
account for the local sweatings and pigmentation. We
know that normal pigment is formed from a particular
product of metabolism of the cutis, being formed both in
the ordinary epithelial cells and in the connective tissue
cells. These connective tissue pigment cells are the
regulators of the metabolic process, as they consume the
surplus pigment-forming substance. The abnormal pig-
mentation of rheumatoid arthritis is probably due to a
local increase in the formation of the normal pigment,
consequent upon some abnormal trophic innervation,
and to a deficient consumption of the surplus by the
connective tissue cells. The vaso-motor changes are in
all probability due to the centre situated in the cells, in
the intermedio-lateral tract, being affected in a similar
fashion to those in the anterior cornua. One of the
greatest points of interest is the tachycardia. Bezanc;on 49
states that tachycardia may in some cases be due to
pressure on the vagus, but he suggests that more often it
is due to the absorption of certain toxines. He cites the
case of the bacillus tuberculosis, and also of certain
staphylococci, streptococci, etc., of the secondary purulent
infection so common in phthisis. Bouchard obtained
from tuberculin a substance to which he gave the name
eetasine, which had the property of producing dilatation
of the vessels. Toxines, with similar powers, have been
obtained from the product of the bacillus pyocyaneus by
Charrin and Gley ; and from those of the staphylococcus
aureus by Arloing. By acting as vaso-dilators these
substances would tend to produce tachycardia, since the
heart tends to act more rapidly as the peripheral friction
diminishes. In other cases the toxines, by giving rise to
a neuritis of the vagus may cause it. Vierordt in a case
of Phthisis found such a neuritis, as evidenced by a great
number of vagus fibres having undergone degeneration
AETIOLOGY AND PATHOLOGY. 41
and atrophy. With regard to the local sweating, it is
probably due to paresis, caused by the toxine acting on
the sudoriferous, and vaso-motor centre of the bulb.
Similar action is seen in influenza (Semmola 51).
It has been found by Hunter 50 that, in all probability,
pernicious anaemia is caused by the presence of bacterial
poisons, just as it has been found to occur from the
presence of cadaveric poisons, and analogous ferments.
Such being the case it requires little imagination to
conceive that a similar process may occur in rheumatoid
arthritis. These bacterial poisons would seem to act by
a hemolytic process which is specially limited in its
action to the portal blood.
With regard to this anaemia there are some points of
interest. These are the diminution of the haemoglobin
value of the red cells and the increase of the white.
Forsbrooke also notes this diminution of the haemoglobin.
According to Ostler we have three classes of anaemia : —
(1,) Those in which the percentage of haemoglobin in
each corpuscle remains the same, and the percentage of
colouring matter corresponds to the percentage of the
corpuscles. This is usually seen in anaemia due to
haemorrhage, or arising from some organic disease. It
may be noted that Laker 54 and Mackenzie 55 both point
out that in malignant disease the haemoglobin value is
decreased. The former states that from this fact alone
one can diagnose the nature of the tumour, at least in
so far as to say it is malignant or benign.
(2,) Those in which the haemoglobin is reduced out of
all proportion to the reduction of the corpuscles, so that
the individual value of each red cell in colouring matter
may be greatly lowered. Chlorosis is the typical example
of this class.
(3,) Those in which the percentage of haemoglobin is
increased, and in which, therefore, the anaemia is not so
42 RHEUMATOID ARTHRITIS.
great as the reduction would appear to indicate. This is
seen most markedly in pernicious anaemia.
In rheumatoid arthritis, then, we have to do with an
anaemia belonging to the second class — in fact an
oligochroniaemia.
We have now to ask ourselves why, in one form of
anaemia, the haemoglobin value should be lessened, and
in another increased ? Where it remains constant it is
probably due to a loss of blood as a whole, whereas, in
the other cases, it must be due to some abnormal con-
dition having a direct influence on the blood cells or
their contents. We know that anaemia implies a want
in the adjustment between the gains and the losses of'
the blood — defective haemogenesis or excessive haemolysis,
the former depending upon deficiencies in quantity
or quality of the food, insanitary surroundings or
mode of life, inherited or aquired defect in the haemo-
poietic viscera etc., and the latter on the processes of
fever and inflammation, or to the presence of deleterious
substances in the blood. With the former condition we
have nothing to do. It would appear as if most forms
of anaemia in which destruction of the red cells and their
contents is the typical feature, must depend, for their
occurrence, on some substance, harmful to their existence,
circulating throughout the system. Dr. Hunter 56 says
that blood destruction is of two kinds — (a) passive,
which is the ultimate destiny of the red corpuscles, and
which being a process of natural decay is evidenced by
the presence of pigment in the spleen, liver and bone-
marrow ; and (b) active, in which the haemoglobin
escapes from the corpuscles into the plasma, and is in
great part excreted by the liver as bile pigment. In
health no trace of this breaking up and excretion of free
haemoglobin is found, but in such a disease as pernicious
anaemia there is abundant evidence in the liver cells.
ETIOLOGY AND PATHOLOGY. 43
This has been found not only in pernicious anaemia but
also in malaria, and as the result of certain poisons
which destroy the blood. Now, this destruction of the
blood would not appear to take place so much in the liver
as one would expect, as in the spleen and to a less extent in
the gastro-intestinal capillaries. This Hunter has demon-
strated by many beautiful experiments. He found that
almost all haemolytic process was stopped by removal of
the spleen, whilst experimenting with toluylenediamin.
The chief function of the liver would, therefore, appear
to be the disposal of the products of haemolysis. He goes
on further to show that certain substances, such as
toluylenediamin, act on the blood indirectly and depend
for their effect on the action of certain cells and especially
of those of the spleen ; whereas such substances as pyro-
galic acid, glycerine, distilled water, etc., act directly,
and depend on the quantity injected for their effect.
This, however, does not help us much in solving the
question as to why, in one case, the same class of poison
should produce an increase in the haemoglobin value,
whilst in another it diminishes it. Are we to suppose
that each individual poison possesses a selective action,
and that it has the power of picking out one constituent
only, of the blood, for special attention ? This is possible
from what we know of the action of bacterial poisons,
but it is hardly probable. It appears to me more likely
that the different classes of bacterial poisons will have
different effects — thus the toxic albumens may have the
power of dissolving out the haemoglobin without destroy-
ing the cell (see the action of snake poison and that of
malaria) and the ptomaines may be more destructive to
the life of a corpuscle than to its contents.
In rheumatism we have an acute disease which is most
probably due to an infective organism (Newsholme) 57
and, in which, Dr. Garrod 5S finds a loss of the red
44 RHEUMATOID ARTHRITIS.
corpuscles with a corresponding loss of haemoglobin — the
corpuscular value remaining constant. In some cases,
daring the course of the disease, there is, however, a
tendency to a decrease in the corpuscle value of a tran-
sitory nature, but which may become more permanent
during convalescence, producing a more or less chronic
anaemia. In malaria, a disease due to an infective
protozoa in all respects resembling a bacterial infection,60
we have, according to many observers (see Mannaberg,61
Evans,59 etc.), a reduction in the haemoglobin value,
especially after the paroxysms. Mannaberg says that
" for several days after the last paroxysm of fever the
proportion of haemoglobin still fell." He gives as explan-
ation of this the supposition that the haemoglobin is
dissolved out by the parasitic poison, dissolved in the
liquor sanguinis. Surgeon Evans 59 notes a reduction in
the number of the red corpuscles, and also of the haemo-
globin— the loss of the latter exceeding that of the
former. He found no change in the number of the white
corpuscles. Finally, in pernicious anaemia, Dr. Hunter
maintains that the anaemia is due to the presence of
bacterial poisons acting on the blood in the portal capil-
laries, thus causing an anaemia in which there is an
increase in the haemoglobin value of the individual cells.
I take it that in the first disease, as there is no
increase in the number of the white corpuscles, we are
dealing with a pure toxaemia — the bacteria themselves
not entering into the blood. And in the second we have
a mixed cause — the parasite not only destroying the cells
and their contents by their presence, but their toxines,
by dissolving out the haemoglobin, produce a diminished
haemoglobin value. And in the last case we are probably
dealing with an alkaloidal poison absorbed from the
intestinal canal. According to Cohnheim 62 certain sub-
stances, of which snake poison is one, has the effect of
vETIOLOGY AND PATHOLOGY. 45
dissolving the blood corpuscles, and Meragliano 63 states
that there are certain pathological conditions in which
the blood serum exercises a destructive influence upon
the red cells, which causes them to give up their hemo-
globin to the menstruum, and that it then disappears
from the blood. In the present state of our knowledge
one does not like to dogmatise, but it would appear to
me as if the two classes of bacterial poisons (ptomaines
and albumoses) had each distinctive actions. In rheuma-
toid arthritis we are dealing with a disease in which the
micro-organisms exist in the blood, but they, as far as
I know, do not live on it as do the malarial parasites,
and that probably, therefore, the anemia is to a great
extent due to their toxic products, dissolved and circu-
lating in the blood.
The increase in the number of white corpuscles is of
interest, as it is found in most infective conditions, and
according to Hunter 64 the increase is roughly propor-
tional to the severity of the disease. Habershon 65 says
he has noticed an increase, not only after the introduc-
tion of alkaline carbonates, but also from the presence of
toxines in the blood. Should bacteria themselves be
present, the destruction of the red cells will probably be
greater and occur sooner than where their products only
exist.
REFERENCES.
1. Heberden. — " Commentaries," Appendix, p. 417.
2. Adams. — ■" On Rheumatic Gout."
3. Fuller. — "Rheumatic Gout and Sciatica," note, p. 335.
4. Charcot.— " Maladies des Vieillards," 2nd Ed. p. 223.YL
5. . Trastour. — "Du Rheumatisme," 1853.
5. Garrod.— " Rheumatism and Rheumatoid Arthritis," p. 238.
7. Garrod. — Loc. cit., p. 239.
8. Haygarth. — " Clin. History of Diseases," 1805.
9. Garrod. — Loc. cit., p. 240.
46 RHEUMATOID ARTHRITIS.
10. Trousseau. —" Clin. Med.," 1865. (Syd. Soc. transl.).
11. Garrod. — Loc. cit., p. 241.
12. Kohts.— " Berlin klin. Wochenschr.," 1873, p. 304.
13. Leyden. — " Klinik der Riickenniarks-krankheiten,'' 1874.
14. Adams. — Loc. cit., p. 15.
15. Sahli. — " Deutclies Arch, fiir Innere Medicin," 1893.
16. Nevvsholme. — " Lancet," vol. i., 1895, p. 661.
17. E wing.— "Lancet," vol. L, 1894, p. 1&36.
18. Fodor.— " Centralb. f. Bakt. u. Parasitenk," Feb. 28, 1895.
19. Pye Smith. — " Guy's Hospital Reports," 1874, xix
20. Hutchinson.—" Pedigree of Diseases."
21. Forsbrooke. — " Dissertation on Osteo-Arthritis."
22. Remak.— " Deutsche Klin." 1863.—" Med. Centralzt.," 1861.
23. Senator. — " Ziemssen's Handbuch," 1875 and 1879.
24. Ord.— "Brit. Med. Journal," vol. ii., 1884, p. 268.
25. Duckworth.—" Brit. Med. Journal," vol. ii., 1884, p. 263.
26. Pitres and Vaillard.— " Rev. de. Medicin," No. 6, 1887. *
27. Duplay and Cazin. — "Arch. Generales," January, 1891.
28. Ord.— Loc. cit.
29. Garrod. — " Treatise on Rheumatism, etc." p. 239.
30. Garrod.— Loc. cit., p. 287.
31. Spender. — " Early symptoms of Osteo-Arthritis."
32. Spender.—" Brit. Med. Journal," vol. i., 1894.
33. Vulpian. — " Lecons sur 'lAppareil Vaso-moteur," 1875.
34. Raymond—" Rev. de Medicin," 1890, p. 374. V
35. Hoffa.— " Volkmann Klin. Vortrage," 1892.
36. Gowers. — " Diseases of the Nervous System," p. 443.-'<»
36a. Massolongo. — "Riforma Medica," vol. ii., 1893, p. 159.
37. Strumpell.— " Munchener Med. Wochensch.," 1888.
38. Sabourin. — " These de Paris," 1873.
39. Darkschewitsch.— " Neur. Cent," 1891, p. 353.
40. Vallat.— " Arch. Generales," 1877.
41. Vidal and Bezaneon. — " Annales de l'lnstitut Pasteur,"
February, 1895.
42. Erb. — "Progressive Muscular Dystrophy."
43. Schafer. — " Brain," vol. xvi., p. 147.
44. Ferrier.— " Brit. Med. Journal," 1893, vol. ii.
45. Folli.— "II Policlinico," December, 1894.
46. Spender.—" Brit. Med. Journal," 1893.
47. Ferrier. — Loc. cit.
48. Duplay and Cazin. — Loc. cit.
49. Bezaneon.--" Revue de Medicin," January, 1894.
50. Hunter.— " Practitioner," 1890 and '89, and "Brit. Med.
Journal," vol. ii., 1892.
51. Semmola. — " Transl. of the Academie de Medicin," 1891 —
1892.
52. Marie P. — " Lectures on Diseases of the Spinal Cord " (Syd.
Soc), p. 236.
53. Marie P. — Quoted Souza Leite in thesis on " Acromegaly,"
(Syd. Soc.) p. 77.
54. Laker.—" Centralb. f. d. Med. Woch.," 1S87, p. 405.
oo
JETIOLOGY AND PATHOLOGY. 47
Mackenzie. — "Brit. Med. Journal," 1891, vol. i.
56. Hunter.—" Brit. Med. Journal," 1889, vol. ii.
57. Newsholme. — Loc. cit.
58. Garrod.— " Brit. Med. Journal," 1892, vol. i., p. 335 and 1139.
59. Evans.—" Brit. Med. Journal," 1891, vol. i., p. 759.
60. Mannaberg. — " Malarial Parasites," (Syd. Soc.,transl.) p. 389.
61. Mannaberg. — Loc. cit., p. 385.
62. Cohnlieim. — " Lect. on General Pathology," (Syd. Soc.
transl.) vol. i., p. 474.
63. Meragliano. — " Berlin Idin. Woch.," 1892, August 1.
64. Hunter.— Loc. cit., 1892, vol. i., p. 1139.
65. Habershon.— " Brit. Med. Journal," 1892, vol. i„ p. 1139.
48
CHAPTER. III.
PATHOLOGICAL ANATOMY AND
BACTERIOLOGY.
Degenerative Character of Changes-Point of Origin — How the
Bacteria gain Access — Naked Eye Appearances — Changes in
Synovial Membrane— Loose Bodies — Ligaments — Characters
of Synovia — Changes in the Cartilages — Cornil and Ranvier's
Views — Erosion — Proliferation — Lipping — Changes in Bones —
Rarefication — Osteo- sclerosis — Volkmann — Changes in the
Muscles — Central Nerve Changes — Peripheral Nerves — Cardiac
Changes — Kidney — Blood — Glands — Fibrous Nodules —
Heberden's Nodes— Situation and Mode of Growth — Gout as
a Cause — Their Nature — Various Observers' Views — Bacteri-
ology— Dr. Blaxall's Report, etc.
On examining the changes after death in Rheumatoid
Arthritis, we are at once struck by the extensive and
degenerative character of the lesions. Much has been
written and said on the subject, but owing to the scarcity
of post-mortem material, until the acute stages at least
are past, few observers agree. Colles l and Todd2 held
that the disease was not inflammatory in nature, whilst
Adams,3 Brodie,4 and Cruveilhier 5 did; Fuller0 looked
upon it as a disorder of nutrition, rather than the result
of inflammation ; and Senator 7 regarded the changes as
partly inflammatory, and partly degenerative, whilst
Garrod8 also takes this view. Bindfleisch9 held that the
disease was essentially one of those lingering inflam-
matory conditions, which accompany the decay of the
organism, like atheromatous disease of the internal coat
of the arteries. He says that the inflammation, not
being powerful enough to cause suppuration, sets up a
hyperplastic over-growth. Trousseau,10 in his clinical
PATHOLOGICAL ANATOMY. 49
lectures, says the synovial membrane demonstrates its
inflammatory origin. From what we know of the
disease its changes must be inflammatory in origin, and
probably begin in the synovial membrane, and spread
from thence to the cartilage and deeper structures. In
acute rheumatoid arthritis the changes are, of course,
principally degenerative or destructive in character; but,
as the disease progresses and becomes more chronic,
there comes to be more and more reparative change
leading to cartilaginous, osteophytic and ligamentous
hardening and overgrowth. As I have said, in the acute
cases, the inflammatory and destructive element is in
excess, whilst in the chronic or osteo-arthritic, the
fibroid or sslerotic is.
Brodie, Adams and others, thought that the disease
eommeneed in the synovial membrane, whilst Yolkmann,
Billroth ll and Garrod consider it starts in the cartilages.
Given a micro-organism circulating in the blood, I think
it probable that the synovial membrane will be the
first to suffer. As the micro-organism is of fairly rapid
growth, especially after gaining access to the joint
fluid, one would expect it to spread rapidly and affect
almost simultaneously, by dissemination, the whole of the
internal surface of the synovial cavity. The question
is, How do the micro-organisms gain access to the joint
cavity in the first instance? The probability is that
they set up an endarteritis in one of the small vessels on
the surface of the synovial membrane, with a diffuse cell
exudation, and this, by extension and rupture, breaks
into the joint cavity, and thus liberates them for further
mischief. As regards this point the experiments by
Chvostek12 are of interest as they show: (1,) That the
walls of blood-vessels, not evidently altered anatomically,
are permeable to bacteria ; (2,) That the anatomical
structure of the synovia and its vessels is an obstacle,
4
5o RHEUMATOID ARTHRITIS.
and bacteria enter the joints considerably later than
they do the kidneys through the renal vessels ;
(3,) That the exit of bacteria depends on (a,) their
kind — - thus a staphylococcus passes most readily,
then a streptococcus, and lastly the bacterium
coli. This is probably due to the virulence of the
micro-organism for the animal, and also to certain
tissues being more liable to certain bacilli than others ;
(b,) their virulence — in tjais .cojinection the action of
toxines must be con#gmi^&-? (fc^ijtet factors, chiefly
nervous — thus c\iui£^ the nerves haQpjs the exit of
bacteria. If this itheor^Ua^orr^atQit- of^Aourse, makes
the synovial memWine far more wily to be primarily
affected than the c^tyage^^^gojvvever,3^/ do not think
one can lay much str^^^if^^i^Jjmion is primarily
affected, nor is it of vital importance.
1. General naked eye appearance of the joint. — We
find an affected joint presents the following general
characteristics : It is swollen and increased in size,
usually, in the acute stages, in a characteristic ovoid
manner ; but which, in the more chronic stages, becomes
less marked and more irregular. In the chronic forms
there is often deformity produced, partly by out-growth
from the cartilages or bones, and partly by twisting or
distortion of the joint ; the deformity may be due to
both or either of these causes. On opening the joint
we probably find some fluid, certainly in the earlier,
and acuter cases almost always. Trousseau remarks that
the joint is often distended by hydrarthrosis. This
presence of synovial fluid during life is often deceptive,
and the doughy or pulpy synovial membrane produces
a feeling difficult to differentiate from that of fluid.
The synovial membrane we notice is thickened — in acute
cases this thickening being soft and pulpy, whilst in
the chronic stages it is hard and dense. The ligaments
PA THOL OGICAL ANA TOM Y. 5 1
are affected in a similar way, and, in very chronic cases,
may present cartilaginous or even bony deposits. The
inner surface of the synovial membrane is injected,
often intensely so, and is granular in appearance. Here
and there small abrasions may be noticed, but they are
seldom of any depth. The villi are thickened, and
more prominent than usual ; this is easily demonstrable
by placing a piece in water, when the villi float up,
showing their character beautifully. The peri-articular
cellular tissue is affected in a similar fashion to its
neighbours. All the soft tissues undergo great develop-
ment of new formed tissue, and the subsequent
contraction and adhesion of which, with the surrounding
parts, give rise to stiffness and limitation of the joint
movements, and finally to fibrous ankylosis. These
adhesions and contractions play a great part in the
development of deformities. On turning to the articular
surfaces we find, if the cartilage be not completely worn
away, as it may be in the chronic ^"~ ~\
cases, that they present a velvety
appearance quite characteristic.
In places will be seen small or
large erosions of the bone, accord- E'
ing to the severity of the case. D
This, in the acute cases, is red,
rarefied, vascular and soft, but
later on becomes sclerosed, hard,
, , , . „ . Fig. 1.— Section thrcmgh pha-
dense and almOSt OI an lVOry COn- laugeal joint in chronic Kheu-
n mi i •-! i matoid Arthritis: A, erosion of
SIStency ; there Will alSO pOSSlbly cartilage; B, thickened mem-
. brane with cartilaginous depo-
be SOme lipping 01* growth Of new sits ;C,eburnatedsiirface of bone
from rubbing of cartilaginoiis
cartilage round the edges of the body ; r>, eburnated articulating
surface; E, thickened soft
articulating surfaces. Beneath tissues.
the cartilage the bone presents, as a rule, a normal
appearance showing that where protected it does not
undergo change. This, however, is not invariably the
52
RHE UMA TOW A R THRITIS.
case, as we now and then see changes going on in
bone protected by cartilage. Such are the appearances
en masse, so now let us study the
individual elements separately.
2. Changes in the synovial mem-
brane and surrounding" parts. —
The synovial membrane, as we
have already mentioned, presents
at first a bright red appearance
from the injection of its vessels,
but in the later stages it becomes
duller, granular and hypertro-
phied ; and, as a whole, much
thickened. Lebert13 mentions a
varicose condition of the vessels
of the synovial membrane, but
, osteophytes; B, *
eburnated bone; C, Grooves on probably he refei'S to a Congested
articulating surfaces (after Bill- r J r>
roth)- condition. The villi become
prominent and hypertrophied ; they may undergo fatty
or cartilaginous degeneration, so that the appear-
ance may be that of a number of pedunculated fatty
polypi, or else of a quantity of dendritic vegetations,
villi, or fingers, some fatty, .and some cartilaginous.
The polypi arise from the budding, and growth of the
normal villi. In the normal state we know that the
synovial membrane is edged by fringes and villi, and
that these have appendages ; and it is from these
fringes that the polypi and other vegetations arise.
These fringes look highly vascular, and have a soft
velvet-like feel. Under the microscope we see that the
synovial cells have undergone proliferation, and that
large numbers of new formed blood-vessels exist, some
full of blood, but all with thickened walls. Scattered
throughout are numbers of small round cells. M.M.
Cornil and Eanvier u state that the cartilage may
PA THOL OGICAL ANA TOM Y. 5 3
be formed in the synovial fringes as follows: "The
normal fat cells in the fringes or villi, undergo degener-
ation, and are replaced by embryonic cells, and whilst
those in centre form cartilage, those at the periphery,
form fibrous tissue." According to Kolliker,15 in the
normal state, cartilage cells exist in the synovial fringes,
and it is more reasonable to suppose that the cartilage
is developed from them, than in the method suggested
by M.M. Cornil and Eanvier. Kindfleisch corrobor-
ates the evidence with regard to the presence of
pedunculated polypi, vegetations, villi, and fringes. As
a rule these only become prominent in the chronic
stages, and this specially refers to the cases where
cartilaginous degeneration has occurred. The pedicles
which fasten those nodules of cartilage to the synovial
membrane, are apt to become stretched, and may in
the end break off, giving rise to loose bodies which lie
free in the cavity of the joint. In very chronic cases,
these cartilaginous bodies may still farther undergo
change, and become ossified. It has also been stated
that loose cartilaginous bodies are found in various
bursas. Personally, I have failed to verify this.
The loose bodies found in Eheumatoid Arthritis may
be classified into: (a,) Melon- seed-like bodies, and
masses of coagulated fibrin, derived from the synovial
surfaces ; (b,) Loose bodies derived from the synovial
membrane, consisting of fully formed tissues, such as
cartilage and bone ; and (c,) Loose bodies derived from the
articular end of the bones, being detached ecchondroses
and osteophytes.
(a,) -seed-like bodies. — Kokitansky 15a refers to
bodies of this kind, and mentions cases in which he has
seen fibrous or fibroid small bodies, varying in size and
shape, projecting from the surface of the synovial
membrane, and which he says can quite conceivably
54 RHEUMATOID ARTHRITIS.
become detached. Again, it is stated that fibrinous
exudation gives rise to both melon-seed bodies, and
to fibrinous masses. A case of the latter is mentioned by
Dr. Logan Turner.45 On microscopical examination
the fibrinous mass was found to consist of fibrin with a
large number of cells, resembling leucocytes, entangled
in its meshes.
(b,) Loose bodies derived from the synovial membrane,
consisting of fully formed bone or cartilage. — Most of
the loose bodies found in rheumatoid joints undoubtedly
arise from abnormal development of the fringes, which
normally exist at the margins of the articular cartilages.
These increase in size and vascularity, giving rise to
sessile and pedunculated bodies, varying in number and
size. During this process the membrane itself undergoes
change, and the connective tissue cells develop into
fibrous tissue, fibro-cartilage, cartilage, and bone. As
time goes on, the connecting pedicle of the peduncu-
lated bodies grows thinner, and finally the body may
drop off, in some cases after a slight sprain or wrench,
but in others during some natural movement of the
joint. These bodies, examined microscopically, present
the character of hyaline cartilage, with here and there
cells undergoing proliferation.
(c,) Loose bodies derived from the articular ends of
the bones, being detached eeehondroses and osteophytes.—
In rheumatoid joints formative changes are constantly
taking place at the periphery, giving rise to nodular
outgrowths of cartilage, and finally by deposition of
lime salts or ossification they become bony. These
nodules may become detached possibly by injury, and
thus lead to such a body existing loose in the joint.
In one such case the body was found to consist of
hyaline cartilage irregularly arranged. In some places it
was proliferating, and in others ossification had begun.
PATHOLOGICAL ANATOMY. 55
The ligaments which form part of the affected joints
become swollen and inflamed, and finally undergo
absorption, or are so replaced by new formed connective
tissue, that it is impossible to trace them on the most
careful dissection. Owing to the cellular tissue under-
going great development, and from the formation of
new connective tissue, adhesions are formed with the
surrounding parts which lead to stiffness and difficulty
in moving the joint, and finally even to fibrous
ankylosis.
Under the microscope the synovial membrane is seen
to be infiltrated with newly formed connective tissue cells,
the blood-vessels are dilated, and their walls thickened,
and here and there are small collections of leucocytes
surrounding them. On proper staining micro-organisms
are discovered scattered
throughout the mem-
brane,but more especially
wherever there are any
collections of round cells.
Similar changes are
1 j ■ i-i ar.ff -,-v^v; Fig. 3.— Diagrammatic sketch of connective
llOieu. m ine SOIL peri- tissue, showing micro-organisms (much en-
articular connective tis- larged)-
sue. In the ligamentous structures, during the acute
stages, the intercellular spaces seem to be increased in
size and number, and a few round cells present them-
selves ; whereas, in the chronic stage, they are replaced
and converted into a mass of dense connective tissue, in
which little or no structure can be traced.
It has often been stated that in Eheumatoid Arthritis
there is no effusion. This however, is quite incorrect,
as again and again have I definitely proved its presence
by tapping a joint. It certainly is present in the most
acute cases, and often in considerable quantities. It is
most often noticed in the knees, wrists, and phalangeal
56 RHEUMATOID ARTHRITIS.
joints. In these latter joints it often forms small, tense,
synovial protrusions, which give the impression of small
elastic bags full of fluid. Broclie, Adams, Fuller, Garrod,
Trousseau and others, have recognised the presence of
fluid, whilst Besnier,10 Senator, and Homolle,17 deny it.
On examining the fluid, Hoppe Sejder ls found that it
contained the following ingredients : —
Mucin
.
18-19
per
thousand,
Albuminous Substances
-
20-92
35
Etherial Extracts
-
•93
Alcoholic ,,
-
1-30
11
Watery ,,
-
•65
H
Acetic ,,
-
1-53
11
Inorganic Substances -
-
8-79
?'
Total 1
Solids
52-31
11
Water
947-69
11
The etherial extracts were cholesterin, lecithin, and
traces of fat. I have found the fluid to be a straw
coloured viscid fluid, with a dash of reddish colouration
(trace of blood), moderately alkaline.
Under the microscope (on cold stage) large numbers
of multinuclear granular corpuscles are seen, very
little, if any, larger than red-blood discs. Most of the
round cells are quiescent, but a considerable number
of irregular ones showed active amoeboid movements.
There were a few rouleaux of red corpuscles, and a
few scattered individual red discs. Also indistinctly
seen are numerous small round bodies, some highly
retractile, and with them a few bodies (very faint),
apparently micro-organisms. On staining, these latter
proved to be so in enormous numbers.
Normal synovial fluid is found to contain in addition
to fat molecules, a few amoeboid corpuscles, as well as
cells similar to those which occur on the projections of
the membrane.19 We thus see that, beyond the micro-
organisms, this fluid differs also in the number of cells
PATHOLOGICAL ANATOMY. 57
present, both amoeboid and granular. The presence of
blood was probably accidental. Dr. Goodhart, as men-
tioned by Dr. Fagge, on one occasion found blood
effused into a rheumatoid joint.
It is very rare to have suppuration, and, in fact, I
know of no case in which it has occurred. Dr. Mansel
Moullin,20 however, reports three such cases. He believes
that the bacteria which caused it reached the joint by
the blood. The disease in all cases began in the soft
parts, and spread from thence to the bones, cartilages,
and ligaments. Dr. J. K. Lunn, also reports one such
case.46
3. Changes in the cartilages. — Many believe that
the first changes begin in the cartilages, but I am not
inclined to agree with them. I think, however, that the
cartilage must be involved at a very early stage. Post-
mortem, we usually find that the whole surface of the
cartilage has suffered, but, if seen early, it is also not
uncommon to find the disease limited to one or more
small patches, from whence it spreads to the surround-
ing areas. Kindfleisch says the cartilage undergoes a
perfectly homologous proliferation, beginning in the
outermost or superficial layers, and gradually extending
to the deeper ; that the cells divide, and group them-
selves into rows of eight to twenty, and go on growing
until the matrix has disappeared, and a tissue made up
of cells or large vesicles results. Billroth says the
intercellular substance does not soften as in inflamma-
tion generally, but that it breaks up into filaments. He
says the changes commence in the cartilage, and spread
from thence to the synovial membrane, and then to the
bone and periosteum.
To the naked eye the first change is a loss of natural
polish, and it comes to present an appearance which has
been likened to velvet. As the disease spreads and
58 RHEUMATOID ARTHRITIS.
becomes more developed, the central parts of the affected
areas break down, and erosions occur which, gradually
extending and deepening, cause the whole of the cartilage
to be absorbed, and the heads of the bones exposed.
As the erosion goes on a new formation of cartilage may
take place round the edge, giving rise to the lipping or
heaping up so often seen in the advanced cases. A. sort
of pseudo-lipping may be observed when the central
portions are erosed down to the bone, whilst the
marginal portions are nearly, if not quite, unaffected.
Close investigation is necessary to distinguish this
alteration. When true lipping does occur, it does not
do so in very regular sequence, but rather does so in
nodules, and it is from this circumstance that the name
" Rheumatisme Noueux," by which it was long known,
was derived. Under the microscope, we find that the
process of disease consists in a proliferation of the
cartilage cells, beginning in the outermost or superficial
layers, and gradually extending to the deeper. The
process was first described by M.M. Cornil and Ranvier.
They show how the cells undergo multiplication,
and form groups of from eight to twenty cells sur-
rounded by capsules, and that in some cases there are
large mother cells, and capsules inside which the
daughter cells develop. Of these some will have
their own capsule, whilst others will be without.
They show how it can be demonstrated, by staining
with iodine, that these cells are not true cartilage cells,
as their capsules only stain very faintly, if at all.
According to them the superficial layer of capsules
swells, and becoming globular bursts, and discharges
their contents into the joint cavity. The capsules in
the next and succeeding rows, being only able to grow
perpendicularly, open into the more superficial rows
forming parallel tubules, and, as time goes on, these
PATHOLOGICAL ANATOMY. 59
burst in turn into the joint leaving the tubules empty
(Eindfleisch and Weber21), whilst the ground substance
or matrix lying between them, becomes separated into
filaments, giving rise to its fibrillated and velvety
appearance. According to Eindfleisch, mucous degener-
ation of the fibrils occurs, causing them to disappear
the more easily, and thus also explaining the presence
of mucin in the joint fluid. I have never been able to
verify this description.
In sections one sees proliferation of the cartilage cells,
but I have never been able to detect any arrangement
into tubules as described by Cornil and Eanvier. Did
it occur, one would expect to find cartilage cells in the
joint fluids. I have never done so with certainty, and I
have examined many cases in the hope of finding them.
Of course, the cells may have undergone so much degen-
eration, and alteration, that they would be unrecognis-
able. What I have seen under the microscope is, round
an erosion, a large number of round cells which penetrate
for some distance into the substance of the cartilage.
In this area the cartilage cells are seen to be proliferat-
ing freely, and the matrix to be disappearing, being
Fig. 4.— Sections through diseased cartilage; A, proliferating cartilage cells;
B, round celled tissue ; C, periarticular loose connective tissue.
eaten away, partly by the round cells, and partly
replaced by the new formed cartilage cells. Deeper
down the proliferation still continues, but in a less
marked way. With regard to the fibrillation of the
60 RHEUMATOID ARTHRITIS.
matrix, the use of staining reagents rather interferes
with one's results, so on that point I can make no
definite statement, but I can emphatically state that
I have never seen anything at all approaching the
drawings which illustrate most of our text books. The
process is one resembling, I take it, all other erosions,
and inflammatory conditions of cartilage. A few
micro-organisms I have always found in the superficial
layers, mixed up with the round celled tissue.
The cells, at the edges of the cartilage, proliferate in
a similar manner. Cornil and Eanvier ascribe the mar-
ginal overgrowth to the fact that the cartilages, at their
margin, are overlapped by a layer of synovial membrane
which prevents the escape of the cellular contents into
the cavity of the joint. The cartilaginous overgrowth
may become converted into osseous tissue, the change
beginning as shown by Volkmann in the layer nearest
the original bone. As a rule, even when seen in the late
stages of the disease, these osteophytes have still a
covering of cartilage. The lipping which is seen in gout
differs from that just described. According to Dr. Wynne
the overgrowths in the latter disease are a sprouting of
the cancellous tissue of the epiphysis, carrying with it
the cartilage, which, however, only covers it as far as
its summit — the rest being covered by fibrous tissue
continuous with that of the periosteum, and synovial
membrane.
4, Changes in the bones. — As the cartilage erodes, and
leaves bare the bone underneath, we have certain changes
occurring. In the acute stages, we find the disease
in the cartilage extends and involves the bone, which
presents a red and vascular appearance. It is soft, and
readily breaks down as the bony constituents are absorbed.
These are replaced by a red, semi-fluid material differing
greatly from the normal marrow. This substance, under
PATHOLOGICAL ANATOMY. 61
the microscope, is found to consist largely of giant cells,
with many nuclei (osteoclasts), in a mass of round cells.
As the disease becomes more chronic we find the bone
comes to present a hard, white, polished, ivory-like sur-
face, to which the term "eburnation" has been applied.
This hard dense layer is thin, and erosions through
it showing the cancellous tissue beneath, presenting
features as above, are not uncommon.
On the surface of the exposed bone, as it hardens, we
see grooves and striae, which are found to correspond
with the eminences, and protuberances,
on the opposing articulating surface (see
Fig. 2). As the result of the processes
of destruction and new growth, the bones
often present a mushroom-like appearance.
Volkmann22 described such a condition,
saying that they looked as if they had
been moulded whilst in a softened con-
dition.
True bony ankylosis rarely occurs,
except in the spinal column (Bowlby). fig. 5.— Metacarpal
.-, j«-i • ™ . bone, showing osteo-
Aclams noticed occasionally hypertrophy phytes (after Billroth),
of the shafts, whilst Broca23 described this as being
chiefly confined to the epiphysis.
Various theories have been advanced to explain the
eburnation. It is, probably, one of Nature's safeguards
to prevent the further inroads of the disease. Zeigler 24
states that, whilst the superficial layers of the cartilage
are proliferating, and becoming fibrillated, a softening
process is going on, in the deeper layers, which leads to
the formation of cavities ; and these becoming filled,
later on, with the vascular medullary substance, which
grows into them from the bone, give rise to ossification.
Cornil and Banvier believe the eburnation to be due to
the discharge into the adjacent medullary spaces of the
62 RHEUMATOID ARTHRITIS.
contents of the most deeply seated cartilage capsules,
which as they enlarge, cause the bone to be absorbed ;
and these cells from the capsules, by a process of osteo-
sclerosis, give rise to the hardened surface. In some
cases they attribute it to the extension of inflammatory
processes to the most superficial layers of the bone.
Some think local osteitis is the principal cause, and
others that it is due entirely to mechanical means, i.e.,
the rubbing of the bones one upon another. The bony
structure of the epiphysis may also be altered.
Volkmann, whose theory is probably correct, has
pointed out that the changes are caused, to his mind, by
a rarefying osteitis followed by an osteosclerosis. That
the wTasting of the bone is not purely mechanical is
proved by the fact that the change sometimes goes on in
parts protected by cartilage.
On examining sections of bone, and also of the medul-
lary tissue, I was struck by the appearance of some of
the cells in the latter. They were large granular cells
with many nuclei, and, in a few instances, I found places
where they occurred in depressions of the bone. From
this circumstance there could be no doubt as to their
nature. They were osteoclasts, and it is evident that the
nature of the process is a rarefying osteitis ; but at the
same time a process of sclerosis, due to osteoblasts, must
either be going on, or else will follow, as the more acute
stage passes off.
I have failed to find micro-organisms in the soft
medullary tissue, but I have no doubt they exist. I find
Gwilt25 mentions that, in this disease, he noticed the
medullary tissue was a great deal more vascular with
proliferation of corpuscles than in the normal. This has
also been noticed by Husse, 26 and Kussmaul.27 If we
compare the medullary substance with that found in
morbus coxae, senilis, wre see that, in the latter disease,
£iiii£
PATHOLOGICAL ANATOMY. 63
which is due almost entirely to a process of absorption,
the bony interstices are filled with a yellow fatty sub-
stance, quite different from the red vascular substance
of rheumatoid disease.
To recapitulate, I would
say, we have an acute
inflammatory disease set
up by micro-organisms
starting in the synovial
membrane, spreading
thence tO the Cartilage, Fig. 6. -Osteoclast eating bone.
bones, and ligaments, causing in the cartilage and bones,
at first an ulcerative or eroding process followed, as the
disease becomes less acute, by hardening and thickening.
This is following all other types of disease, and explains,
perfectly, all the post-mortem appearances as well as all
the symptoms.
Before leaving this division of the subject, let us con-
sider some other points of interest.
5, Changes in the muscles. — The principal change is a
well marked atrophy of the muscle substance which
affects the whole of the muscle, and not only a part of it.
There is no diminution in the number of the fibres, but
each fibre is found to be lessened in size. As a whole
the muscle presents, what Debove 2S calls, the colour of
dead leaves. In a few cases degeneration of the muscles
has been found, showing itself by longitudinal striation
with proliferation of the sheath nuclei, and increase of
the interstitial tissue (Vallat).29 This change, probably,
only occurs in those cases in which inflammatory
changes have spread from the joint to the muscles,
nerves, or central nerve system.
6, Changes in the central nerve system. — The only
changes, hitherto noticed, have been an atrophy of the
motor cells in the anterior cornua in several cases, seen
64
RHE UMA TOW A R THR1TIS.
by Folli.30
specimens
this one,
I have only been successful in obtaining
from the nerve system in one case. In
on examining the spinal cord, I found
degeneration, and vacuola-
tion 31 and 32 of the ganglion
cells of the anterior cornua.
The vacuolation of nerve
cells consists in the appear-
ance, within the nerve cell,
of oval or perfectly spheroidal
bodies of high refractile
power quite unaffected by
any staining reagent, colour-
less, but lustrous. In many
cases this quality is wanting,
and it is then evident that
the spheroidal outline is of
a genuine cavity or vacuole
from which the former con-
tents have escaped by rupture.
The removal of the contents
of such vacuoles may be
effected during life by the
lymph connective system.
The protoplasm surrounding
t.-multipolar gaxgliox Cells the vacuoles is, more or less,
in a state of granular degen-
eration. The degeneration,
and the feeble staining, indi-
cate a fatty change in the
cell protoplasm. The sig-
nificance of this is understood when we realize
that fatty degeneration and vacuolation indicate a
change in the blood corpuscles, leading to defective
oxygenation. We see examples of this in chronic pul-
FlG.
X 350-
FROM AnTKRIOR CORNUA.
/ 1 Cell swollen with bright trail s-
' lucent contents.
2 a, Vacuoles with degenerated
cell ; b, Granular degeneration.
'3 and 4 show vacuolation, seen
also in
5 and 6, in degenerated cells, and
t 7 swollen degenerated cell.
PA THOL OGICA L A NA TOM Y.
65
monary affections, alcoholic states, and from the effect
of certain poisons (arsenic, phosphorus, etc.), or any of
the many circumstances which restrict the supply of
oxygen to the tissues. Those elements naturally suffer
earliest, and most, whose nutrition is carried on at the
greatest disadvantage. The exact importance of this
occurrence cannot at present be accurately estimated, but
shortly I hope to obtain farther and certain evidence.
Massolongo 32a refers to changes in the anterior cornua
observed by Klippel, but does not particularise them.
7. Changes in the nerves. — In a certain number of
cases peripheral neuritis has been noticed, but in so few
as to negative any idea that
this is the cause of the disease.
It is almost certain that it is
set up by an extension of the
inflammation from the joint
lesions. Pitres and Vaillard 33
report some cases where they
found such a condition of the
nerves, and they express the
opinion that these changes
cannot be the cause of the
joint lesions. In other cases
again we find that the spinal
cord and nerve roots have
been affected by a spinal
arthritis, probably by com-
pression and narrowing of
the foramina. In these cases we may have a descending
neuritis. I have been fortunate enough to obtain sections
from the nerves, in a case of rheumatoid disease which
had undoubtably given rise to a secondary neuritis.
There could be no doubt that it was secondary. Under
the microscope there was an infiltration of small round
Fig. 8. — Portion of nerve in which
there was neuritis : A, thickened con-
nective tissue, nucleated ; B, nerve
bundles greatly diminished in size;
C, blood-vessels with thickened walls.
66 RHE UMA TOW A R THRITIS.
cells in the nerve sheath, around the vessels, and
amongst the nerve fibres themselves, especially in the
neighbourhood of the sheath. Thickening of the endo-
neural septa, and of the interfibrillary substance, was
also seen ; and there was a thickening of the intima of the
blood-vessels, which encroached upon the lumen of the
vessel.
8. Changes in the heart. — Lesions of the endocardium
and pericardium are comparatively rare, but not
so rare as is thought. MM. Charcot and Cornil
mention numerous cases in which changes were present,
and with no rheumatic history, and in which the lesions
developed after rheumatoid joint troubles. Any valve
may be affected, but my experience has been that the
disease is almost entirely confined to the mitral valves.
I find out of 78 cases, of which I give an analysis, 14
had cardiac troubles. I have had no opportunity of
examining such cases post-mortem, but other writers
state that the affected areas present a hardening, and
thickening, with vascularity, and present small vegeta-
tions upon their surfaces. Pericarditis has occurred in
several instances.
9. Changes in the kidneys. — Charcot and Trousseau
lay special stress on the occurrence of chronic albuminous
nephritis, but I think it is a much rarer complication
than they would lead one to suppose, at least in this
country.
10. Changes in the blood. — In almost 95 per cent, we
find anaemia exists in a greater or lesser degree. The
blood, under these circumstances, presents the following
characters. There is a slight, but well marked diminu-
tion in the number of red blood corpuscles, a marked
diminution in the haemoglobin, and a slight increase in
the number of the white corpuscles. The percentage of
the diminution of the red corpuscles ranges from 85 per
PATHOLOGICAL AAA TOM Y. 67
cent, to 56 per cent.; whereas that of the hemoglobin
does so from 80 per cent, to 45 per cent. It is thus
evident that the haemoglobin value of each corpuscle is
lessened. The percentage increase of the white corpuscles
is small. The blood showed red corpuscles of varying size
and varying shapes, but did not present any microcytes nor
yet any nucleated corpuscles. The haemoglobin appears to
be less in quantity in each cell, as well as in a less stable
union with the cell stroma. It crystallizes out more
readily and is more easily acted upon by such substances
as common salt, acetic acid and sulphate of soda in
solution. There is a difficulty sometimes in distinguishing
between a swollen red cell with its haemoglobin dissolved
out and a white cell. This might account for the
variability in the estimation of the number of the latter.
11. Changes in the glands. — As one would expect, we
find in the glands of the arm pit and groin, some
enlargement, but there is none in the spleen. This
enlargement is such as is found in other bacterial
diseases, and consists of a chronic hyperplasia.
12. Fibrous nodules, although more common in acute
or chronic rheumatism, are not unknown. They consist
of round celled tissue which, probably, originates in an
endarteritis. Dr. Pitt 34 describes such a condition, and
mentions that this endarteritis may account for the cold
extremities so often seen in this disease. Nepven35
describes a nodule formed round a vessel with small dis-
integrating clots. Cavafy 36 mentions that the nodules
are vascular in origin. A subject now crops up of much
interest, namely, the relationship between chronic rheu-
matoid arthritis, and what are known as Heberden's
nodes. These are small enlargements or osteophytic
outgrowths from the normal nodules, present round the
articular surfaces of the bones of the hand. They were
first described by Heberden 3T who gave it as his opinion
68 RHEUMATOID ARTHRITIS.
that they had nothing whatever to do with gout. This
has been, and still is, a much vexed question. As these
nodes may occur in the more chronic forms of polyar-
ticular rheumatoid arthritis we have to ask ourselves
what their relationship to this disease may be.
They occur, as I have said, as small rounded nodular
growths, usually arising from the third phalanges, but
sometimes from the second. They are painless, and
have no tendency to ulcerate, and though they some-
what interfere with the movements of the fingers, yet
they are more disfiguring than painful. The nodes may
be the only symptom of disease present, but they are
more usually associated with a generalised disease.
They may precede or follow such a disease. On examina-
tion they are found to consist of an outgrowth from the
bony tissue, and are covered by a hernial process or
projection of the synovial membrane, forming a pouch or
bag, which, as a rule, contains fluid, and acts much as
a bursa. On microscopical examination, they are found
to be formed of true bone. It is found that these nodes,
usually, as Heberden says, present themselves in elderly
people of the female sex, above 60 years of age ; but I
have seen them well developed in patients of 40. At
first, we find that the third joint is enlarged, and as a
whole, and not only on one aspect. On the dorsum of
the finger the furrows which mark the normal joint are
seen to have disappeared, and are replaced by an
elevation — the whole joint forming a distinct thickening.
This can be detected on the palmar aspect as well. The
enlargement of the bones is not confined always to one
phalanx, but both of the opposing phalanges may be
affected. This enlargement goes on until we have a small
tumour, obviously growing from the bone, about the size
of a pea, over which glides, possibly, a burse or synovial
pouch. The development of these nodes is accompanied
PATHOLOGICAL ANATOMY. 69
by peculiar sensations in the fingers, such as numbness,
and they are often accompanied by pain on pressure, or
on movement. They may, however, be quite painless,
and even if not so, the pain is never severe. When
they become quiescent the pain goes completely. If the
disease is not arrested, the movements of the joints
become much interfered with, and ankylosis may finally
result. When nodes are present in rheumatoid arthritis
we find that deformities seem to develop specially early,
and to be more persistent. The usual deformity is de-
flection of the terminal phalanges towards the radial
side, and this is rendered more conspicuous by the
deflection of the finger, as a whole, to the ulnar side.
Are these growths then the ordinary osteophytic out-
growths, so common in rheumatoid arthritis, or are they
something different ? Some assert that they are true
gouty formations, and others that they have nothing-
whatever to do with gout, but are by nature a form of
rheumatoid arthritis. Heberden, as I have said, main-
tained that they were not gouty, as he had seen them in
people who had never been affected with gout. Begbie38
differed from him entirely, and says they are intimately
connected with gout. He stated that he had watched
their development from the first, being sometimes the
result of an inflammatory affection, more or less acute,
and attended with the constitutional disturbance which
marks the fit of gout ; but more commonly they were the
consequence of a slow, and chronic gouty disorder. He
also says he had never seen them except in those suffering
from gout or from the gouty diathesis. Charcot,39 on the
other hand, agreed with Heberden, and denied that they
had any connection whatever with gout. He stated that
it was a form of rheumatoid arthritis, and that the ana-
tomical changes were those of this disease. Sir A. B.
Garrod 40 stated that he had seldom seen them in patients
70 RHEUMATOID ARTHRITIS.
suffering from true gout, and agreed with Heberden's view,
with regard to them. Dr. A. E. Garrod 41 is of the same
opinion, but says he has seen them in cases with clear his-
tories of gout, and no other arthritic affection. Duck-
worth 42 believes that they are of a true gouty nature, and
says that the changes, found by Charcot, were frequently
of an undoubted gouty nature. In gout he has seen true
ankylosis result from the deposit of urates, and exostoses
may also be caused thereby. Lecorche 43 also takes this
view. Pfeiffer44 maintains that it is a symptom of true
gout, as he has seen them arise in cases of gout, and in
cases where uratic deposits existed, but he admits that
he has also found them in people in whom there was no
gout. Personally, I have seen these nodes most frequently
in chronic rheumatoid arthritis, never in the acute forms;
but I have also seen them in true gout. Is it not possible
that they may be common to both diseases. They are
unquestionably the result of some irritation giving rise
to an increased, and morbid growth in the normal
nodules ; so why should not this irritation have its origin
as much in the poison of one disease as in the other ? I
have seen a considerable number of such cases, and I
have in no instance found any deposit of gouty material
in the nodules. They have always been of pure bony
substance, but this, of course, does not invalidate the
argument that the gouty poison may have originally
started the morbid process.
The accompanying photograph {Plate I) was taken
by J. W. Gifford, Esq., of Chard, the patient being an
inmate of the Bath Eoyal Mineral Waters Hospital, and
through whose kindness I am permitted to publish it.
The patient, a lad of 20, was the subject of acute rheu-
matoid arthritis — the synovial swellings being marked.
A small sesamoid bone can be distinguished on the
inner side of the first metacarpophalangeal joint.
PLATE I.
Photograph of the Bones of the hand in a case of Rheumatoid Arthritis.
BACTERIOLOGY 71
What is of special interest, however, is the fact,
that in the acute stages no bony outgrowth occurs.
Indeed, as this photograph shows, there is, if anything,
a diminution in the size of the bone, as may be seen in
the heads of the metacarpals — which have a rounded off
appearance not seen in the normal bone. This is
specially noticeable in the second metacarpal at its ulnar
side, the disease in this joint being specially acute.
The deformity of the little finger was due to contraction
of the flexor tendons, with atony of the extensors.
Bacteeiology.
For some time before the actual discovery of the micro-
organisms, Dr. Wohlmann and I, looking at the clinical
nature of the disease, and at the course of the symptoms,
had practically made up our minds that the disease was
microbic in character. The absence of iiost-mortem
material complicated the case, but in the absence of this
material, we decided to obtain what specimens we could
from the living subjects. In this way we were led to
aspirate affected joints, and examine the fluids so
obtained microscopically and by cultivation. On stain-
ing we were readily successful in determining a micro-
organism was present, but at the same time were troubled
with the difficulty in staining it properly, and getting
it free from precipitate. However, we, to a certain
extent, overcame these difficulties, and got fairly good
results with carbo-fuchsine and methyl-blue, sufficiently
so to satisfy ourselves that it was a micro-organism we
were dealing with. Our first culture attempts utterly
failed, but by degrees we got fair results. Our apparatus
was deficient, and this led in most instances to the
growths dying out in the course of from three to four
weeks' time. We obtained growths on blood-serum, agar-
agar, and on beef bouillon. The bacillus, for to us it
72 RHEUMATOID ARTHRITIS.
appeared to be a dumb-bell shaped bacillus, is about 2//,
long, the ends staining deeply, the connecting portion
not at all. In fact in many cases it resembles a diplo-
coccus. It appears to grow more freely when it has a
plentiful supply of air, possibly pointing to a greater
need of oxygen. In all, we found it in 24 cases out of 25
examined. We also found it in several pieces of synovial
membrane obtained during aspiration and in the car-
tilages, synovial membrane, and periarticular tissues in
the few sections we were fortunate enough in obtaining.
On Dr. Blaxall's suggestion we examined the blood in
some of the acute cases, and in several were successful
in finding it by microscopic examination, but never so
characteristically as to warrant one in diagnosing the
disease from that alone.
Having arrived at this stage, and feeling the utter
inadequacy of our apparatus, I felt compelled to call to
our assistance more skilled aid, and Dr. Blaxall of the
British Institute of Preventive Medicine, kindly under-
took the duty. For the last eighteen months he has
been working hard at the elucidation of its life-history,
and the result we see in the following report* : —
" This investigation was undertaken at the request of Dr.
Bannatyne, of Bath, who stated, that he, with Dr. Wohlmann,
had arrived at the conclusion from the clinical aspect of cases
suffering from rheumatoid arthritis, that the disease was due
to a micro-organism, and further that by microscopic examina-
tion of the synovial fluid from affected joints, they had found
an organism, constant and distinct, and this mirco-organism
they considered to be specific.
" Synovial fluid from affected joints, was sent me from Bath;
the fluid was aspirated with antiseptic and aseptic precautions,
with such success that out of eighteen cases which have been
submitted to me, only twice have I found it contaminated.
* This report appeared in the "Lancet," April 25th, 1896.
BACTERIOLOGY. 73
" My first attempts to obtain organisms in the synovia and
to obtain cultivations from it, resulted in failure. I adopted
the ordinary methods of bacteriological procedure, staining
films of the synovial fluid for a few minutes with aniline dyes,
and inoculating serum tubes and all ordinary culture media,
as well as making plate cultivations of nutrient agar-agar and
gelatine after Koch's method. But I was unable to observe
any organisms in the microscopic specimens, or to recognize
any appearance of growth upon any of the culture media.
" I then varied the staining methods, leaving the specimens
in the dyes for a prolonged time in the cold, applying heat,
and using concentrated solutions. By these means organisms
could be perceived in the specimens corresponding exactly to
those described by Drs. Bannatyne and Wohlmann, and
morphologically identical with those seen in their microscopic
specimens. But their recognition was unsatisfactory, owing
to several causes. In the first place, it was evident that the
organisms took up the stains with great difficulty, and only by
their prolonged action, or by the application of heat; but these
means resulted in a very dense colouration of the synovial film.
Secondly, they were decolourized with great ease, for attempts
to decolourize the substratum left the organisms unstained.
" Again, the microbe being very minute, it was exceedingly
difficult in heavily stained specimens to discriminate it from
cUlris or from precipitate of the dye used. It was necessary
then to find a method, by which the organism should be well
stained, should retain the stain, and yet allow the synovial
film to be sufficiently decolourized, and one that should obviate
all precipitate of the dye. I cannot claim to have attained
this result, but after many trials I have adopted the following
procedure as being most satisfactory.
"A thin film of synovial fluid, draAvn out between two cover-
glasses, is dried over the flame and fixed in the usual way, by
passing through the flame five or six times, as otherwise the
organisms are apt to be washed out. The cover-glass is then
immersed in dilute acetic acid for about two minutes, well
washed with water and dried again, this second drying being
74 RHEUMATOID ARTHRITIS.
to prevent the cover-glass sinking in the staining fluid. The
stain which I have found most useful is aniline methylene
blue. The cover-glass is placed, specimen side down, on a
watch-glassful of the stain, and the whole placed in a moist
chamber, in the dark, for three to five days. It is then washed
in gently running water for some hours, rinsed in distilled
water, dried and mounted in the usual way. More expeditious,
though not giving such clear and well defined specimens are
aniline gentian violet and carbolic fuchsine. This latter stain
I have found it advantageous to dilute one-third with distilled
water. Twelve to thirty-six hours are sufficient for these, in a
moist chamber. The cover-glasses are washed in running
water in the same way, then well rinsed with thirty per cent,
alcohol, washed in distilled water, dried and mounted. The
acetic acid clears the synovial film and allows the dye to
penetrate more readily. The prolonged staining deeply colours
the organisms, so that the washing process leaves them well
stained, though the film is decolourized ; and the moist chamber,
by preventing the evaporation of the dye, obviates the
precipitate.
"Microscopic examination of the specimens reveals an or
ganism possessing peculiar characteristics. At first-sight it
appears to be a diplococcus, the two cocci being distinctly
stained, but separated by a clear unstained interval — about
equal in length to the diameter of either stained end. This
interval I have never succeeded in staining. But careful
observation will show, especially where the substratum is
faintly coloured, that the intervening portion is nearly as
broad as the diameter of either stained extremity, and that it
has parallel contours. I therefore consider the organism to be
a bacillus, which exhibits very marked polar staining. The
average length is 2/x and the average breadth "6^, but this
latter measurement varies greatly with the intensity of the
staining. But the organism, as seen under the microscope,
appears much smaller than the measurements would indicate,
owing to the limited portions stained.
"The number of organisms met with in a cover-glass specimen
BACTERIOLOGY. 75
of synovial fluid from a joint, affected with rheumatoid ar-
thritis, varies greatly. Sometimes the field is crowded with
them; at other times they are scattered and hard to find.
These differences appear to follow very closely the acuteness or
chronicity of the disease.
" The organisms are generally evenly distributed through the
film, showing, however, a tendency to congregate around the
leucocytes. Their arrangement is always discrete; I have
never seen chains or masses formed.
" Though the staining methods mentioned above have given
me the most satisfactory specimens, yet the organisms can be
seen when stained for a much shorter time, especially with
gentian violet, methyl-violet, or carbolic fuchsine. But it is
found that these stains if allowed to evaporate, deposit upon
the cover-glass a precipitate of dye, which so closely resembles
the organism, that it is by no means easy to recognize them
when but few are present in a preparation so observed — be-
cause after such a brief staining, attempts to remove the pre-
cipitate by washing and the use of re-agents, bring about more
or less completely the clecolourization of the organism; whereas
after a longer contact with the stain, the microbes are coloured
more firmly, and are less easily decolourized. But there is
one exception to this statement, in a method which I have
devised and found useful.
" Impressed with the small size of the organism and the
minute portion stained, it occurred to me that the protoplasm
might take up dyes more readily if it came into contact with
them while moist. With this in view, I mixed a drop of
synovial fluid with a few drops of the stain (aniline methylene
blue being best) on a cover-glass, and rubbed out with a
platinum needle. The cover-glass, with the stain and synovial
fluid together, was then dried slowly over a burner, and when
quite dry, fixed by passing several times through the flame,
then freely washed with water, dried and mounted. In this
way I obtained very fair results, the greater part of the stain
being washed off, leaving the organism well coloured. For
rapid diagnosis, this method is very useful.
y6 RHEUMATOID ARTHRITIS.
" Treated by Gram's method, the organism is almost com-
pletely decolourized.
" I have been able also to detect the organism in the synovial
fluid in the hanging drop specimen, but this is far from easy,
unless they were present in larger numbers.
" I have now stained and examined the synovial fluid from
various joints from eighteen cases affected with rheumatoid
arthritis, and in every case have observed the organism which
I have described above (see Plate II, Fig. A) ; but in fluids
from distended joints, due to other causes, as chronic synovitis,
gonorrhceal and tubercular affections, I have entirely failed to
find them.
Cultivation.
"At first all attempts at cultivation, both aerobic and an-
aerobic, yielded apparently no result. But I imagined that
this might be due in part to the small size of the organism,
so that if it formed colonies they might be scarcely per-
ceptible, and judging from the scattered distribution in
synovia that the tendency to a free growth might be small,
and in part to a slow development. Keeping these points in
view I resolved to try it upon a large scale, and in such a
manner, that any change in the medium might be easily
detected. Into litre and half-litre flasks were put 250 ccs. of
peptone beef-broth, filtered repeatedly until it presented a
perfectly clear and bright appearance. Great care was taken
over this to avoid the slightest obscuration. The flasks were
sterilized and placed in an incubator kept at blood heat for
several days to prove their sterility, and also to be sure that
the fluid remained perfectly clear. If these conditions were
fulfilled, the flasks were carefully opened, and a drop or two
of synovial fluid from an affected joint allowed to enter.
The flasks were then incubated at blood heat. Similar flasks,
but uninoculated were also incubated at the same time to
serve as controls.
" I was fortunate enough to attain success with the first
experiment. The first point noticed was that for three days
PLATE II.
Fir/. ..{.-Synovial fluid, stained with gentian violet, x 900.
Fig. 5.— Beef- broth culture, stained with carbolic fuchsine, x 900.
BACTERIOLOGY. 77
the beef-broth remained perfectly clear, pointing strongly to
the conclusion that the synovial fluid contained no ordinary
organism. But, from the fourth day and onwards, there
could be seen floating in the clear fluid very minute particles,
and these increasing gave rise to an appearance resembling
" gold dust." This effect was enhanced by lightly shaking the
flask. Sometimes the growth seems to stop at this "gold dust"'
stage, but at other times it may become slightly flocculent,
recalling to mind the appearance of a commencing growth of
tubercle bacilli in glycerine beef-broth. The beef-broth never
becomes turbid, but always retains its bright appearance.
" The control flasks showed no such development. Micro-
scopic examination of such a culture, stained as before, displays
the organisms in considerable numbers, but it can be readily
understood from the delicate nature of the cultures and the
imperfections of staining methods, that a too great reliance on
stained specimens was not advisable, and that additional
evidence would be helpful.
" Verification was obtained by making hanging drop speci-
mens, and this is the easiest method of demonstrating the
presence of the organism.
" In the hanging drop, the microbe appears, precisely as in
the stained specimens, with two bright refractile ends, and an
intermediate part much less obvious. They may occur in
zoogloea masses, or as discrete individuals hugging the edge
of the drop. They are non-motile, but have a marked oscil-
latory movement. I have been fortunate enough to see them
undergo division in the hanging drop specimen.
"The intervening portion lengthens out, the ends appearing
to pull against one another energetically, and the whole organism
oscillating the while uneasily. The middle part lengthens out
more and more, so that the organism appears to be about
twice its ordinary length ; then suddenly the link snaps, and
freed ends fly off in contrary directions, and are lost amidst
their fellows.
" This phenomenon helps, I think, to explain some variations
in length frequently noticed in stained specimens from culture.
78 RHEUMATOID ARTHRITIS.
In these some bacilli will be seen very short, the stained ends
quite close together, with a minute unstained connecting link,
very suggestive of a diplococcus.
" These I take to be quite young organisms. Some, however,
are much longer, attaining a length of 3/x, or possibly 4//,
the stained edges widely separated, and a clear unstained
sheath faintly visible with the highest powers. These I
imagine to be the older forms, soon about to divide. In these
older forms too, the staining is sometimes somewhat different.
Instead of the staining portion being more or less spherical
at the ends of the organism, the coloured part is in the form
of a conical cap, the base towards the centre of the bacillus, and
spreading faintly down the edges of the sheath. These forms
show best the claim of the organism to be considered a bacillus.
It will be obvious, however, that it is very difficult to bring
out these subtle differences in a photograph — and indeed the
limited staining of the organism and its minuteness, render the
production of good photographs by no means easy (see Plate II,
Fig. B).
"The organism also grows upon nutrient agar-agar. If beef-
broth cultures are inoculated on tubes of sloping nutrient
agar -agar, and incubated at blood heat, growth takes place in
about three days, and in a very characteristic manner. This
growth is exceedingly delicate. It appears no more than as a
fine transparent film, which under a lens can be seen to consist
of minute colonies no larger than a pin point, and perfectly
transparent. To the naked eye it bears a very close resem-
blance to condensation water, though control tubes and the
obvious tests show that this is not the case.
" It grows also in Loffler's serum, but here the growth is even
more difficult to recognize owing perhaps to the opalescence
of the medium. It occurs as minute points, less difficult to
observe at the lower part of the tube, where the condensation
water has washed off the cholesterin. Stained cover-glass speci-
mens, and hanging drop specimens made from such cultures,
reveal an organism identical morphologically with that des-
cribed as present in the beef-broth cultures and synovial fluid.
BA CTERIOLOG Y. 79
" I have also grown the organism in milk, where it appears
to nourish, but without causing curdling, or precipitation of
the casein. On nutrient gelatine, however, at 22° a, I have
never succeeded in getting a growth, and in liquid gelatine
incubated at 37° C. there is no visible growth.
" Examination of the blood in cases affected with rheumatoid
arthritis has also afforded me positive results of the presence
of the organism.
" I have examined the blood taken near to an affected joint,
and also that from a distance, and in both have been able to
detect the organism in microscopic specimens. Out of five
specimens of blood submitted to me, I have been successful in
three, and these were the most severe cases. But further
proof of the presence of the organism in the blood is the fact
that twice I have been able to obtain cultures from it. The
method was the same as previously described. The blood
was inoculated into flasks of clear sterilized beef-broth and
inoculated at blood heat temperature. Subcultures were also
made from these flasks on to agar-agar and blood-serum. The
organism found was identical in every respect with that which
grew from the synovial fluid, and with that which was
observed in the stained specimens.
" Some animal experiments have been made, for which I am
indebted to the Council of the Royal College of Surgeons, and
to Dr. J. Sims Woodhead. Two ccms. were injected subcu-
taneously into mice, guinea-pigs, and rabbits, but without a
fatal result. There is some reason to think, however, that the
cultures set up a disease in rabbits, which affected the joints;
but further experiments are necessary to arrive at the truth
with regard to this matter.
"As far as I am aware only one organism has been previously
associated with rheumatoid arthritis, which it is necessary to
discuss. This was described by Schuller.* He writes of a
bacillus 2-6yu long and '75— '995/x broad, which exhibits polar
staining. It is easily coloured by ordinary stains, especially
* Max Schiiller : "Berliner Klinisch. Wochenschrif t, " Septem-
ber 4th, 1393.
8o RHEUMATOID ARTHRITIS.
carbolic fuchsine, but very easily decolourized. It is
noteworthy that Schiiller thinks it incumbent on him to
point out the distinction between his organism and tubercle
bacilli.
" It grows readily upon gelatine at 25° c. In two, three, or
six days, small white grains or knobs appear. The gelatine is
liquified, and eventually the organism grows to such an extent,
that tho whole mass becomes opaque white. On agar-agar ic
grows as greyish white flecks or films.
" It is obvious that the organism described by Schiiller differs
markedly from the one under discussion. In fact the only
points of resemblance are the polar staining and the easy dis-
colorization. It therefore appears to me to be indisputable
that this organism of Schiiller's is not that which was dis-
covered by Drs. Bannatyne and Wohlmann.
" To sum up : —
"(1,) In the synovial fluid in eighteen cases of rheumatoid
arthritis an organism has been demonstrated, which is constant
in its characteristics.
" (2,) The organism is a minute bacillus, exhibiting
marked polar staining. It is difficult to stain and easily
decolourized.
" (3,) The organism can be grown in culture media, and pre-
sents striking characteristics. In beef-broth it gives the
appearance of gold dust ; and on agar-agar and serum its
growth is almost invisible.
" It does not grow on nutrient gelatine at ordinary tem-
perature.
" (4,) It is present in the blood of severe cases.
" (5,) It has not been found in the synovial fluid from
distended joints due to other causes.
" It should be added, that it has been impossible to examine
sections of the synovial membrane, owing to the want of
pathological specimens.
" In conclusion I should like to record my thanks to Mr.
Barnard, for the care and skill he has expended on the
photographs."
BACTERIOLOGY. 8;
This report not only corroborates what Dr. Wohlmann
and I had previously determined, but it carries us much
further. The staining methods, as described, and cul-
ture experiments, are the labour of months, and may be
safely recommended to all those who would pursue the
subject further.
To summarise, I may say, we have found a constant
microbe presenting marked peculiarities in all but one
of the cases examined, this one failure being easily
explainable on account of our deficient methods and
knowledge. We have not succeeded by re-inoculation as
yet in producing the original disease in animals, but the
experiments have been so few as to be of little or no
value (what results have been obtained are on our side).
As far as I know the disease is practically unknown
amongst them, and, in fact, they may be naturally
immune. The subject is one of great interest, but, as
will be gathered from the foregoing, of considerable
difficulty.
REFERENCES.
1. Colles. — Quoted Garrod, "Rheumatism and Rheumatoid
Arthritis," p. 274.
2. Todd.—" On Gout and Rheumatism," 1843.
3. Adams.—" On Rheumatic Gout," 1873.
4. Brodie.— " Diseases of the Joints," 1833.
5. Cruveilheir. — "Anat. Pathologique," Lee. ix.
6. Fuller. — "Rheumatism, Rheumatic Gout and Sciatica," 1852.
7. Senator. — " Ziemsson's Handbuch."
8. Garrod. — "Treatise on Rheumatism and Rheumatoid
Arthritis"
9. Rindfleisch. — " Pathological Histology."
10. Trousseau. — " Lect. on Clinical Medicine," (Syd. Soc.transl.)
11. Billroth. — "Gen. Surgical Pathology and Therapeutics,"
(transl).
12. Chvostek.— " Wien. klin. Wochenschrift," June 27, 1895.
13. Lcbert.— " Handbuch der Pract. Med." 1859, ii.
14. Cornil and Ranvier. — " Manual of Pathological Histology,"
vol. i., 1892.
15. Kolliker. — " Elements of Human Histology."
82 RHEUMATOID ARTHRITIS.
15a. Rokitansky. — " Path. Anatomy," Sydeuham Society, vol. iii.,
p. 289.
16. Besnier. — " Diet. Encylop. des Sciences Med." 1876, p. 155.
17. Homolle--" Diet, de Med. and Chir. Prat." 1882.
18. Hoppe Seyler.— " Virchow's Arch." 1872.
19. " Qnain's Anatomy," 9th edit., p. 219.
20. Monllin, M.— " Lancet," 1891, vol. ii., p. 125.
21. Weber. — " Journal of Nervous and Mental Dis." New York,
1884.
22. Volkmann. — " Handbuch der Chirurgie," Band ii., p. 555.
23. Broca.--" Bull, de la Soc. Anatom." xxv., 1850.
24. Ziegler.— " Virchow's Archiv." 1877, lxx., p. 592.
25. Gwilt. -" Handbuch der Path. Anat." p. 1,000.
26. Husse.— " Zeitschrift flir Rat. Med." vol. v., p. 192.
27. Kussmaul. — " Arch, ftir Physiolog. Heilkunde," vol. xi., 1852.
28. Debove.— " Prog. Med." 1880, p. 1011.
29. Vallat— " Arch. Generates de Med." 1877.
30. Folli.— " II Policlimco," December, 1894.
31. Voit and Bauer. — " Zeitschrift fiir Biologie," vii.
32. Trzebinski. — " Arch, fiir Path. Anat. u. Phvsiolog. u. fiir Klin.
Med." Bd. cvii., Heft 1.
32a. Massolongo.— " Riforma Medica," 1893, vol. ii., p. 159.
33. Pitres and Vaillard.— " Revue de Med.," 1887, No. 6.
34. Pitt.—" Clin. Soc. Trans.," vol. xxvii., 1894, p. 54.
35. Nepven. — " Comptes rendus de Soc. de biologie," Paris,
1890, vol. ii., p. 328.
36. Cavafy.— " Path. Trans.," 1883, p. 41.
37. Heberden. — " Commentaries," 1804.
38. Begbie.— Contrib. to " Practical Medicine," 1862, p. 28.
39. Charcot. — " (Euvres Completes," tome, vii., 1889, p. 217.
40. Garrod, Sir A. B.— " Gout and Rheumatic Gout," 1876, p. 503.
41. Garrod, Dr. A. E. — "Rheumatism and Rheumatoid
Arthritis," 1890, 266.
42. Duckworth, Sir Dyce.— " Treatise on Gout," 1889, p. 71.
43. Lecorche.— " Traite de la Goutte," 1884, p. 122.
44. Pfeiffer.— " Lancet," vol. i., 1891, p. 819.
45. Turner. — " Edin. Hosp. Re£)orts," vol. iii., p. 627.
46. Lunn.— " Lancet," vol. i., 1896, p. 294.
S3
CHAPTEE IV.
VARIETIES AND DIAGNOSIS.
Errors in Diagnosis — Acute Rheumatoid Arthritis — Osteo-
Arthritis — Charcot's Classification — Post-Rheumatic, Gonor-
rheal and Gouty Forms— Acute and Sub-acute Rheumatoid
Arthritis — Infantile Arthritis — In Children— In Adults —
Differences — Symptoms — Appearances of Joints — Chronic
Rheumatoid Arthritis — Age — -Appearances— Bony Changes —
Diagnosis between it and Nerve Diseases — Charcot's Disease —
Rheumatism — Gout — Chronic Rheumatism, etc.
l.-VARIETIES.
Peobably Eheumatoicl Arthritis is responsible for more
errors in diagnosis than almost any other form of
known disease. This not only arises from the difficulty
in recognising the disease from certain forms of rheu-
matism and gout, but also because under the name
rheumatoid arthritis several forms of disease have been,
and still are classified. A further differentiation is
greatly to be desired, not only on account of the
treatment, but likewise for prognostic purposes. It has
been my lot to see annually a large number of cases
sent to Bath for treatment, and to which, in the greater
proportion of cases, the wrong name is given. Most
confusion arises apparently between what is, and what
is not chronic rheumatism, the larger proportion of
cases, thus designated, being cases of rheumatoid
disease; and, again, there often is confusion between
rheumatoid arthritis, and some forms of chronic gout.
With care one can usually differentiate between these
conditions, but it is not always easy to do so straight
off.
84 RHEUMATOID ARTHRITIS.
It is my intention to divide the disease into two
sections. In one : (a,) I will class all those acute and
sub-acute cases characterised by inflammatory changes
in the joints — ulceration and erosion of the cartilages
and bones, muscular atrophy, and by other nerve and
trophic phenomena ; and, in the other (b,) all those
chronic cases characterised by a slowly progressive
thickening and hardening of all the joint structures, by
the development of deformities, by the formation of
osteophytes, and by the lipping of cartilage, etc. Owing
to the bony changes and to the general thickened
character of the joints, it is to this form of the disease,
rather than to the acuter, that I would more especially
confine the term osteoarthritis.
My plan of sub-division then is as follows : —
I. Acute Rheumatoid Arthritis, divided into the (a,)
Acute, and (b,) Sub-acute forms, and
II. Chronic Rheumatoid Arthritis or Osteo-Arthritis.
Now, for a moment, let us glance at the other forms
of classification hitherto adopted — most of them being-
based on that of Charcot.1 His method was as follows: —
1. Rheumatisme Artieulaire Chronique primitif general-
ise ou progressif (the Rheumatisme Noueux of others). —
This group is distinguished by the disease having a
tendency to become general, by the small joints of the
extremities, such as those of the hand, and, especi-
ally of the metacarpo-phalangeal, being symmetrically
affected, and, by the fact, that during the progress of the
disease, most of the other joints are successively attacked
in a definite order, and for the most part the mischief
is irreparable.
2. Rheumatisme Artieulaire Chronique primitif fixe on
partial. — In this group the disease is usually localised
to one or two of the larger joints, producing deep seated
mischief. It is sometimes called arthrite seehe or
morbus eoxse senilis.
VARIETIES. 85
3. Nodosites d' Heberden.- — This group contains those
cases usually classed amongst gouty affections, and
confined either to the extreme joints of the fingers, or
else to the next row, leaving, as a rule, the metacarpo-
phalangeal joints free.
More latterly, Dr. Garrod2 has qualified this classi-
fication by adding a fourth group of cases which occur
subsequent to attacks of acute rheumatism, gout, or
gonorrheal arthritis. These two classifications form
the basis of all subsequent ones, and for all practical
purposes are efficient. On one point I dissent from both
writers, and in fact from all English authors, and this is
with regard to Morbus Coxae Senilis. This form of
disease I hold, is not true rheumatoidal, and, therefore,
I have omitted it from my classification.
Before proceeding further, allow me to refer briefly,
to those forms of rheumatoid arthritis which occur
secondary, to some acute arthritic attack. In spite of
being secondary in nature, they present all the charac-
teristics of the primary forms, and, after a few remarks,
will be classed, and considered, with them.
(«,) Post Rheumatic Form. — As has been already
stated, rheumatoid disease is a frequent sequela of acute
attacks of rheumatism. Some observers hold that
the rheumatoidal attack is merely the continuation of
the rheumatic changes ; but, of recent years, other
views have been advanced and accepted. We have come
to understand how any acute arthritic attack lays the joint
tissues open to a subsequent attack of the same disease,
and also to one of some other disease. What is curious
is, that a disease originally limited to one joint should
render the patient liable to a generalised disease — yet
such is the case. This rather points to some blood
condition, than to one entirely dependent on a local
joint state. McArdle3 points this out, and I have often
86 RHEUMATOID ARTHRITIS.
proved the truth of his observation. If Ave believe, as
I do, that both rheumatism and rheumatoid arthritis
are caused by infective organisms, or by their elaborated
poisons, we can more readily understand, and appre-
ciate, the significance of this rather remarkable fact.
Schuller 4 goes the length of proving that the rheumatic
poison renders the joints and constitution more liable
to be affected by rheumatoid arthritis. This probably
also applies to as great an extent in the case of gout,
gonorrhoea, or indeed, to any infective form of arthritis.
In post-rheumatic forms, we find an increased tendency
to the occurrence of visceral lesions.
(b,) Post Gouty Forms. — Hutchinson 5 mentions such
cases as proof of his theory, as to the nature and origin
of the disease. Garrod supports the view that it is a
common sequela, but Sir Dyce Duckworth disagrees
with it entirely. The latter holds that all deformities
and distortions, met with in uratic arthritis, are due
entirely to gout. With regard to their clinical features,
he says, they in many ways resemble those of rheuma-
toid arthritis.
(c,) Post Gonorrheal Form. — The occurrence of rheu-
matoid changes, after a gonorrheal arthritis, is naturally
much rarer than that following a rheumatic attack.
It, however, does occur, and has been mentioned in the
writings of Charcot, Lorain,6 who gave it the name
Rheumatisme blenorrhagique a forme noueux, Sir Alfred
Garrod, Dr. A. E. Garrod, and others.
Just as one form of bacteria, by being antagonistic
to another, prevents the development of the latter,
in the presence of the former, so we would expect to
find the converse ; and not only during the period of
their activity, but after their attack has passed, they
may either have so exhausted the body's natural
protective powers, or else, by the presence of a toxine or
VARIETIES. 87
ferment, so have paralysed this power, as to. render
the system an easy prey to an otherwise innocuous
attack. We might expect that one micro-organism,
if it did not afford immunity, would render the joints
doubly liable to the attacks of another organism, having
a somewhat similar nature, and a somewhat similar
action. As yet we are only on the borderland of know-
ledge of such subjects, and one's remarks must perforce
contain a large amount of what is, as yet, pure
supposition. We know nothing for certain.
While on this subject, I may mention again Drs.
Ewing's7 and Foclor's8 experiments, showing that
anything which reduces the alkalinity of the blood,
reduces its germicidal power. Now we have in this a
clue to the action of bacteria in this disease when it
follows on rheumatism and gout. In both these latter,
the blood's alkalinity is notoriously decreased. What with
the reduced alkalinity, and the destructive action of the
primary poison, we can understand how easily the tissues
may come under the influence of secondary infections.
I. — Acute Eheumatoid Arthritis.
In this division come all cases, acute and sub-acute,
seen alike in the young, and in the grown up ; occurring
either as a primary disease, or secondary to some other
form of arthritis, or to injury. In these forms it is
always poly-articular. Although occurring at any period
of life, the acuteness of the disorder varies largely with
the age of the individual attacked. In children it
rarely is chronic, but tends to assume a rapidly pro-
gressive character, only differing from the acute form
seen in adults, by its more frequent fatal termination.
In young adults it also is usually acute or sub- acute.
In elderly people acuteness is rarely seen, but, in this
respect, it makes up by its intractableness.
88 RHEUMATOID ARTHRITIS.
(a,) Acute Rheumatoid Arthritis. — Fuller 9 was the
first to point out the characteristics of this form, and
subsequently Garrod drew attention to it, pointing
out various things to be noted in the differential
diagnosis between it and acute rheumatism. Both he
and Fuller draw attention to its obstinacy, to the
character of its articular swellings, and to the liability
of certain joints to be involved. Some deny that this
form exists, holding that it is only a modification of
acute rheumatism, but, although, if care be not ex-
ercised it lends itself to much confusion, yet, to one
who has studied the two diseases, no confusion is
possible. In rheumatoid arthritis the disease involves
the bones, cartilages, synovial membrane, and ligaments,
and is accompanied by well marked atrophy, trophic,
vaso-motor, and other nerve phenomena, which render
it quite distinctive and characteristic. In children, we
must carefully distinguish it from those cases of
multiple nerve arthrites — a few of which have been
recorded. These are so similar to what one would
expect in rheumatoid disease, that I am almost tempted
to believe, that they are cases of this disorder, only,
occurring in a somewhat unusual manner. Pasteur10
mentions such a case, in which there was no enlarge-
ment of the ends of the bones, but there was arthritis,
accompanied by a hide-bound condition of the skin.
Barlow n reports another such case, in which there were
subcutaneous nodules. One must remember that
arthritis has been known to arise in scleroderma, and
scleroderma in rheumatoid arthritis. Jaccoud12 mentions
a class of cases somewhat similar, under the name of
Rheumatisme fibreux. Wagner13 also has described
similar cases. From examinations, these joints show
little change in the cartilages, but fibrous bands develop
across the joints, and greatly restrict their movements,
Er-
VARIETIES. 89
as well as lead, by slow contraction to great deformity.
There is always great doubt as to what we are dealing
with in such cases, but one must always bear in mind
that arthritic changes are fairly common, as the result
of spinal degenerative changes. Such being the case,
great care is not only necessary in the diagnosis, but in
the treatment.
Acute rheumatoid al disease is undoubtedly more
important from the clinical standpoint, than the average
chronic case. What makes these cases so interesting is
the age at which they occur, children and young adults,
being for the most part affected. We find it usually com-
mences in one joint, probably one of the metacarpo-
phalangeal ones. It does not remain long confined to
this one joint, but spreads like wild-fire, to most of the
other joints of the body. It shows a wonderful
symmetry not only in the joints affected, but, to a less
extent in the degree. Symmetry is also seen in the
other phenomena present. The joints are swollen,
presenting a characteristic, ovoid or spindle shaped
enlargement, painful and tender to the touch, and hot.
On palpation, they either feel resistent and elastic (Plate
III, Fig. A), with distinct fluctuation, or else they feel
as if they had undergone maceration. The ligaments
and other joint structures being soft, and doughy, and
admitting of a finger tip being sunk into the joints,
between the heads of the bones ; they at times feel as if
they would drop apart (Plate III, Fig. B). The second
condition is in all probability secondary to the first — the
cartilages, and other joint structures being destroyed,
whilst the acute inflammatory condition still exists.
Later on it will become harder again as cicatrisation
occurs. This feeling, and that of tense resistance, are
quite characteristic. Along with this the extremities
feel cold, and look blue, being bathed in a cold clammy
90 RHE UMA TOW A R THRIT1S.
perspiration, although the body temperature is raised
generally. Eecent pigmentations, and other integu-
mentary abnormalities, develop on the face, body, and
forearms, etc., whilst all the time a progressive muscular
atrophy is occurring. The affected muscles are not merely
those in the immediate neighbourhood of the diseased
joints, or even distal to them, but may be situated on
the proximal side as well. A characteristic selection of
the muscles is observed, the atrophy is accompanied by
cramps, and fibrillary twitchings, with, sometimes,
increase of the reflexes, but, unless peripheral neuritis
has been set up, no reaction of degeneration. As the
case progresses the pain becomes greater, worse probably
at night, and on movement of the joint ; the movement
also gradually becomes more and more limited. No sleep
may be obtainable, except by the use of powerful hyp-
notics, and the disease becomes more and more distressing
to watch and to treat. Cardiac abnormalities are fairly
common, and we have other visceral derangements.
The question of its occurrence in children is of interest.
The disease as seen in them is usually very acute, and pre-
sents all the symptoms as seen in adults. The youngest
child I have seen affected was a boy, aged four, the next,
also a boy, aged seven (Plate F), and the next a girl, aged
eight (Plate IV). Undoubted cases have been recorded
by Sir Alfred Garrod,14 Lecaze Dori,15 Monocoro,16 Dr. A.
E. Garrod, Lloyd Davies,17 etc. In his diseases of
children, Dr. Money 18 mentions that rheumatoid
arthritis is seen in children, and that it may follow
on an acute attack of rheumatism : that it may affect
both the feet and hands, and resemble the multiple
joint affection of middle aged women, rather than the
arthritis sicca of the old. The propensit}^, he says,
to deformities and ankylosis in awkward positions is
rather great. Henoch, in his book on diseases of chil-
VARIETIES. 91
dren, also mentions certain cases of apparently rheuma-
toid disease, but he, like many foreign observers, does
not differentiate between it and chronic rheumatic
arthritis.
(&,) Sub-aeute Rheumatoid Arthritis. — This also is
most common in children, and young adults, and is
seen more rarely in elderly people. As a rule, it occurs
only as a stage of a more acute attack, but, of course,
it may from the first be sub-acute in nature. It is
marked by all the symptoms of the acuter form in a
milder degree, with super-added greater liability to
deformities and distortions. The muscular wasting is
as marked, but there is greater cicatricial thickening
of the synovial membrane and ligaments, leading to
adhesions and deformities (Plate VII, Fig. A). There is
increased osteophytic formation, the heads of the bones
enlarging until they assume the mushroom-like appear-
ance of the typically chronic case. There is less synovial
fluid present, and we now get crepitation and grating on
movement, most often of the coarser variety. It is
rarely fatal, but tends to gradually become more and
more chronic, assuming all the characteristics of the
latter form.
II. — Cheonic Rheumatoid Akthritis or Osteo-Arthritis.
In this form it may arise per se, and be always
chronic ; or it may be only the later stages of an acute
attack ; or it may follow on some other form of arthri-
tis ; or as the result of injury. It may affect many
joints, or it may be confined to only one or two. As a
primary disease it is most often seen in middle aged,
and elderly women. It is characterised by great
hardening and thickening of the joint tissues, both
soft and hard ; by eburnation of bone ; by erosion of
the cartilages ; by osteophytic deposits ; by cartilaginous
92 RHEUMATOID ARTHRITIS.
overgrowths and new deposits ; by lipping, etc. There
is consequently much deformity, distortion, and stiffness.
This latter varies, as in one case it may be of the
slightest, whilst in another, it may resist all treatment,
and end in ankylosis. Pain as a rule is not acute,
being more of a constant, gnawing, or wearying charac-
ter. One joint only may be affected, and in which it
may remain, or it may advance steadily from joint to
joint, causing great crippling, not only from deformity,
but from fixing and ankylosis. One marked feature is
the absence of fever, of almost all heat in the joints,
and by the absence of the trophic and nerve changes.
It looks as if the sclerosis or condensation of the bones
and tissues, so peculiar to this condition, had given them
power to resist not only the inroads of the micro-
organisms, but the absorption of their toxines. We
must in these cases discount all the trophic and nerve
abnormalities of the acuter stages and those arising
from disuse. In many respects in Eheumatoid Arthritis
one sees resemblances to phthisis, but in none more so
than between the acute and chronic forms, for, have we
not an almost analogous condition between phthisis and
fibroid phthisis ?
2.-DIAGN0SIS.
From Charcot's Joint Disease it may be distinguished
clinically, by the absence of the nerve symptoms so well
marked in that disease, especially the muscular inco-
ordination, etc., and by the fact that the joint changes in
tabes are marked by the suddenness of the onset ; by
the absence of pain ; by the large quantity of fluid in
the joint ; by the fact that the joint changes at first are
always atrophic, although they may later on become
hypertrophic, and by the increased mobility.
From other nerve arthropathies by the absence in
>
-3
Cxi
DIAGNOSIS. 93
them of pain, and by the presence of well marked nerve
symptoms.
From Syringomyelia, by the formation of new bone
in rheumatoid arthritis being confined to the interior
of the joint capsule, while in syringomyelia and other
spinal arthropathies there may be extreme ossification
of the periarticular soft parts (Volkmann). This cannot
be relied upon, however, as in the chronic cases of
rheumatoid arthritis there may be considerable formation
of bone in the adjacent tendons, ligaments, bursse,
etc.
From Pulmonary Hypertrophic Osteo-arthropathy, by
the presence of pulmonary troubles in that disease,
and by the changes being almost entirely confined to
the bones. Until more is known of this disease we
are not in a favourable position to lay down strict laws
with regard to its differential diagnosis.
From Acute Rheumatism there is little difficulty in
making a diagnosis, except in those rare cases of Eheu-
matoid Arthritis, where several joints become acutely
inflamed at one time. The whole history of the case
is otherwise different. Its preponderating frequency in
women is a point of importance. Apart from this, the
general clinical features of the arthritis are quite
different ; while acute rheumatism begins in the medium
sized joints and spreads to the smaller, rheumatoid
arthritis begins in the smaller and spreads to the
larger. The former too is migratory and uncertain in
its extension ; the latter is slowly progressive, with a
greater tendency to symmetry. The pyrexia of acute
rheumatism, the perspiration, the greater liability to
cardiac complications, are all characteristic. The real
difficulties arise in sub-acute, and chronic cases, when
the joint must be minutely examined so as to make out
that the stiffness, swelling, and deformity, depend upon
94 RHEUMATOID ARTHRITIS.
a general thickening of the textures about the joints,
and not on destructive changes in the joint.
From Chronic Gout the distinction is made by noting
the previous history, and by careful examination of the
joints. Besides the fact of its greater frequency in men
in middle life, whose habits and mode of life contribute
to bring it on, there is usually an account of previous
acute attacks in the joints, mostly the great toe, and, while
in the course of time other joints are affected, the disease
cannot be said to have the same progressive character
and symmetrical spread. The joint changes too are
different. Urate of soda deposits may be noticed in, or
about the joint, as well as elsewhere, as in the ears, etc.
What is quite certain is that the destruction of inter-
articular cartilage, and alterations in the ends of the
bones in rheumatoid disease, are not due to previous
gouty deposits.
A point to be noted in diagnosis is the muscular
atrophy, which presents the following peculiar and
typical features : —
1. It is most marked in the muscles in the immediate
neighbourhood of the joints (interossei, etc.).
2. It is not infrequently found to have affected
muscles beyond this region (trapezius, deltoid pec-
torals, etc.).
3. It improves, and tends to disappear if the joint
trouble ceases, although it would seem to persist at
times long afterwards.
4. It is sometimes accompanied by changes in the
electrical excitability of the muscles.
DIAGNOSIS.
95
o
is
Inflammatory thicken -
ing of the joint tissues,
with deposits of Urate
of Sodium, but does not
tend to destroy tissues.
Most common in men.
CO
■+=
O
CO
a
II
o
CO
Uric acid always pres-
ent, either in blood or
deposited in tissues.
Chiefly affects great
toe.
CO
«!
a
B
tf
o
d
K
b
O
Has little tendency
to the destruction of the
joint tissues, and no ten-
dency to the formation
of bony and cartilaginous
deposits.
1
1
1
1
1
i
1
CD
-4-3
O
CO
-t-3
O
CO
l—i
1
i
!
1
1
i
1
1
c3
CO
c3
u
-4-3
CD
a
a
>>
CO
O
s
CO
s
a
B
O
Affects only the fibrous
tissues, and is marked
by great synovial disten-
sion, pain, and heat.
° q
CD O
S3
.a o
-4-=
>VcO
'eg co
CO ^
L) co
^ co
1
1
1
CD
CD
O
CO
co" CD
I
ra I
.2 5
3 f
c6
ft t
a.=
o -
CO P
3
■i
^4
Q
-1
i
1
3
2
"I l-H
j .2
2 -+3
u
CD
>
CO
q
.2
'co
CD
O
nd O
^ c
q a
o
o
1
1
1
!
i
1
1
1
Does not affect neck
and jaw as a rule, and
symmetry not so marked.
co
CO
co CD
1-1 3
CO ?■
M C
C
co
3
a
a
p
s
D
S
3
Inflammation quickly
involves cartilages and
bones, and, in chronic
cases, is characterised
by great new formation
of tissue.
co
o
CD
CO i-H
+3
CD S
o q
q co
° a
co CD
o g
^ CD
CD
.a
q
o
a
1
o
o
-4-3
^ IS
a
CD
q
o
c6
CO
-4J
O
q
°3 CD
£ S
Q q
o
o
'q
o
CO
.2
"02 q
CP o
a
.5 o
CO j^
CO
Acute form accompan-
ied by muscular atrophy,
and many trophic phe-
nomena.
1
1
1
1
Is specially liable to
to affect small joints, neck
and jaw symmetrically.
i—i
CM
CO
^
iO
8D
C~
CO
Oi
96 RHEUMATOID ARTHRITIS.
REFERENCES.
1. Charcot. — " Maladies des Vieillards."
2. Garrod. — "Rheumatism and Rheumatoid Arthritis," p. 236.
3. McArdle.—" Dublin Med. Journal," 1885, lxix., p. 490,
and lxx., p. 398.
4. Schiiller.— " Med. Record," Sept. 23rd, 1893.
5. Hutchinson. — "Med. Times and Gazette," 1881, vol. i.
6. Lorain.— "Union Medicale," 1866, xxxii., p. 617.
7. Ewing.— "Lancet," vol. i., 1894, p. 1336.
8. Fodor. — "Centralb. f. Bakt. u. Parasitenk.," Feb. 28th,
1995.
9. Fuller. — "Rheumatism, Rheumatic Gout and Sciatica,"
1852.
10. Pasteur. — " Clin. Soc. Trans," vol. xxii.
11. Barlow. — Quoted Garrod, loc. cit. p. 247.
12. Jaccoud. — " Le9ons de Clin. Med.," 1867, le<;on, xxiii., p.
598.
13. Wagner.—" Mlinchener Med. Wochenschr.," 1888.
14. Garrod, Sir A. — " Rheumatism and Rheumatic Gout."
15. Lecaze Dori. — " These de Paris," 1882.
16. Monocoro — " Rheumatisme Chronique Noueux des
Enfants," 1880.
17. Lloyd Davies.— " Lancet," vol. ii., 1893 p. 928.
18. Money. — "Diseases of Children," p. 130.
PLATE VI,
Fig. A. Shows cartilaginous and bony enlargements of the heads of the bones,
with considerable synovial swelling and thickening. Atrophy is marked . K — Shows
thickening of wrist joint.
Fig. B. — Ulnar deflection in a chronic case.
CHAPTER V.
SYMPTOMS AND PROGNOSIS.
Premonitory Symptoms — Spender — Primary Symptoms due to
Micro-organisms — Appearance of Joints — Heat of Skin — Ar-
thrite Seche — Synovial Pouches — Joints first Affected — Sym-
metry — Ankylosis — ■ Deformities — Dislocations — Osteophytic
Oat -growths — Forms of the Deformities — In the Hands and
Knees — Its Causes — Difference in Acute and Chronic Cases —
Cardiac Symptoms — Endocarditis — Pericarditis— Changes in
the Glands — Secondary Symptoms — Muscular Atrophy — Its
Characters — Selective Power — Myotatic Irritability — Fever —
Pulse Rate — Tachycardia — Tension — Anaemia — Haemorrhages
— Purpura — Neuritis — Its Frequency — Trophic Phenomena —
Skin Changes — Glossy Skin — Loss of Hair — Atrophy — Downy-
growth of Hair — Pigmentation — Sweating — Dyspepsia — Kid-
ney— Cardiac troubles — Prognosis.
1. — Symptoms.
As a rule, in every disease we find some salient and
constant symptoms which may be taken to represent
individual disorders — for without them we would have
no characteristic abnormalities. It is so in Rheumatoid
Arthritis. In this disease the joint symptoms are charac-
teristic and constant ; but besides, and as will be seen
later, the character and number of them, and the number
of the structures attacked, all suggest a systemic disease
of some blood poison.
The symptoms may be divided into
A. -Premonitory Symptoms ;
B.— Primary Symptoms, due to the direct effect of the
micro-organisms themselves, and
C— Secondary Symptoms, due to the absorption of
toxines elaborated by the micro-organisms.
7
98 RHEUMATOID ARTHRITIS.
A.— The Premonitory Symptoms.
The disease, in many cases, has no premonitory
symptoms, the first indication of anything being wrong
in the joint being slight pain, with some swelling, and
tenderness on pressure, or on movement. Should, how-
ever, premonitory symptoms be present, they usually
present themselves in the form of numbness, tingling,
or other abnormal sensation of the extremities. Howard,1
Homolle,2 and Garrod,3 all mention such cases. Howard
compares them with the abnormal sensations noticed in
spinal disease. Garrod quotes cases in which there was
a history of sensations of pins and needles in the arms
and hands, and growing pains in the bones. In my ex-
perience I have never been able to get a really reliable
history of any premonitory symptom. I have had
patients say they felt abnormal sensations, but on further
investigation I have found that there has almost invari-
ably been some antecedent trouble which has caused
such confusion as to make their evidence quite unreliable.
Patients naturally pay more attention to such sensations
than they do to a trivial pain or swelling of a finger
joint or knuckle. I think, therefore, we may dismiss
from our minds, as not of much importance, the
premonitory symptoms. Before leaving the subject,
however, I must mention the symptoms described by
Dr. Spender,4 which according to him, if not actually pre-
monitory, occur very early after the onset of the disease.
The symptoms referred to are various vaso-motor and
trophic disturbances, which will be discussed more fully
later on, and pain. The pain on which he lays such stress
is one occurring in the ball of the thumb, and on the
inner side of the wrist. He considers it to be of great
importance, and almost pathognomonic, and it may be
accompanied by a feeling, described by patients, as of
being ''parboiled, scalded, stung all over with nettles,"
PLATE VII.
Fig. A. Shows deflection of left hand. There is complete dislocation of 1st
phalanx of index finger on to palmar surface of metacarpal, and partial of
'2nd phalanx on to palmar surface of 1st ring finger.
Fig. B. Showing spindle shaped swelling of phalangeal joints.
SYMPTOMS. 99
etc. The pains themselves are various in character, but
those of a neuralgic character are common and
characteristic. They are more often referred to the
bones than to the joints themselves.
Given then a disease ushered in by the foregoing pre-
monitory sensations, or by neuralgic pains, it is not long
before we find evidence of the disease in the joints
themselves ; and, following on the joint symptoms, come
atrophy of the muscles with, at shorter or longer
intervals, certain other symptoms due, for the most
part, to derangement of the nervous and vaso-motor
systems. The occurrence of certain changes in the joints,
with or without these other symptoms, then, constitutes
the disease called rheumatoid arthritis. Of the local
symptoms, of course, the most important are those
referable to the joints.
B.— Primary or essential Symptoms.
1. Symptoms due to the presence of the micro-organisms
in the joints. — To the eye the earliest symptom is some
enlargement of one or more joints. This may vary in
degree from the most trivial swelling to an enormous
distension. It assumes all sorts of shapes, and charac-
teristics, and the skin covering the joints may be subject
to many, and various trophic changes. Apart from the
trophic changes it may be reddened, but more often pre-
sents a bluish, asphyxiated look quite characteristic.
As a rule, the shape is more or less characteristic in so
far as the joint alone is affected, but should the tendons
or their sheaths have undergone rheumatoid changes one
can never say what the alteration may be. In an
ordinary case then the joint will be more or less spindle-
shaped, merging gradually into the tissue above and
below {Plate VII, Fig. B, and Plate III, Fig. A).
In acute cases, we may have such an enlargement, due
either to the presence of fluid, or else to pulpy swell-
ioo RHEUMATOID ARTHRITIS.
ing of the synovial membrane ; or again, we may find
that the swelling is not symmetrically spindle-shaped,
and there are what seem to be pseudo-depressions between
the heads of the bones, due to these latter being pushed
apart by the swollen joint tissue, and to the general
softening of the ligaments and tendons (Plate III, Fig. B) .
In chronic cases the enlargement is usually more irregular,
and may, from the enlargement of the heads of the
bones, and from the presence of nodules of osteophyte
growth, as well as from the swelling of the synovial
membrane and presence of fluid, present an enormous
and irregular enlargement. As the disease commences
in the synovial membrane it is not until the later stages,
of the acute, or in the chronic form that we see much
bony enlargement (Plate VI, Fig. A).
Owing to cystic enlargements, or bursse, certain aspects
of the joint may be increased in size out of all proportion
to the rest. In many cases the mapping out of the syn-
ovial sacs is very perfect, from the swelling being almost
entirely confined to them, and, in such cases, the enlarge-
ment is sharply demarcated from the surrounding tissues.
While the acute stage is still in progress, to the
touch the joints feel hot — the temperature often
being raised l°-2° Fahr. above that of the surround-
ing surfaces.
As to the eye, so to the touch, we find three con-
ditions : —
(a,) A tense, elastic, and resistant swelling with
distinct fluctuation, often with secondary sac-like
protrusions of synovial membrane — best seen in the
joints of the fingers, and evidently caused by the
presence of a considerable quantity of fluid under
some tension.
(b,) A soft flabby doughy feeling, as if joints, ligaments,
and all the surrounding tissue had undergone maceration.
SYMPTOMS. 101
Over the joint cavity there is a sort of depression in the
middle of the otherwise generalised swelling, and every-
thing feels doughy or pulpy. There is seldom much
fluid present in such cases, but they are most acutely
progressive. It is usually a secondary stage of the acute
form, and shows that much dis-organisation of the joint
has taken place.
(c,) The third condition is that described by the French
under the name, " Arthrite Seche." In these cases the
joints are enlarged and nodular, and one feels that the
heads of the bones have undergone enlargement ; the
synovial membrane is doughy; there is much crepitation
on movement ; joints can with difficulty be moved, and
this even, if passive, causes much pain; and there may
be ankylosis. It is usually a sequel of the more acute
stages.
At first, on passive movement, there may be little or
no pain, and there may be no tenderness ; but pain in the
acute forms soon becomes marked, and persistent both on
movement, and at rest, especially at night. On move-
ment in the drier, and more chronic forms, we get grating
on moving the heads of the bones one over another.
This may become quite a marked feature. At first it
resembles fine crepitation, but soon passes into the
coarser varieties which only cease from total inability to
move the joint.
During the first stages the skin over the joints may be
reddened, and dusky in hue, along with the other symp-
toms of acute trouble, and in the later we see various
trophic changes, such as " glossy " skin, increase of
pigment, etc.
With regard to the pouches or cysts seen either
in connection with, or in proximity to, a joint, Mr.
Morant Baker5 says that they arise from the synovial
cavities by a process of distention. The synovial fluid
102 RHEUMATOID ARTHRITIS.
on reaching a certain degree of tension finds its way out
into the tissues in the direction of least resistance. It
does so either through some normal channel, such as
that by which a bursa communicates with a joint, or
else by the formation of a hernial projection of synovial
membrane. Finally it pushes its way into, and between,
the tissues until its boundaries come to be formed by the
muscles and other surrounding tissues. I have often seen
such pouches gradually being pushed through the tissues
surrounding the joints, and one can readily understand
how they might have their communication with the joint
cut off either by pressure, from the quickly enlarging
joint, or else by a twist, or by some inflammatory process.
I do not think that these synovial pouches ever actually
burst. On puncturing them I have, more than once,
seen the escape of all the fluid from a joint ; and, on
pressure, one can make them disappear with a temporary
increase of the fluid in the joint.
With regard to the presence of fluid in the joints :
in almost all the acute cases it is present, often in large
amount. However, with the synovial membrane and
ligaments in a state of softening and degeneration, it is
not always easy to differentiate between the two condi-
tions. Haemorrhages into the joints are rare, but not
altogether unknown. Suppuration is even rarer, and I
have never seen it (see p. 57).
In the acute forms of rheumatoid arthritis the
small joints of the hand are those most liable to be
affected by the rheumatoid changes. They are usually
the joints first affected, and often form the starting
point from which it spreads all over the body. It
not infrequently happens, however, that the disease
is not only confined to the fingers, but to the terminal
interphalangeal, or even one terminal interphalangeal
joint.
SYMPTOMS. 103
Charcot gives the following statistics from 45 cases, as
to its origin 6 : —
25, or 55*5 per cent., started in the small joints of the hands,
and feet first.
4, or 8*8 ,, started in the great toe first.
7, or 17*7 ,, started in the hands and feet at the same
time as in a larger joint.
9, or 20*0 ,, started in the larger joints first.
He says the arthritis, as a rule, spreads from the
periphery to the centre; the fingers first being affected,
then the elbows, and then the shoulders. In young
patients he says it is usually general from the first, and
that it is only in the elderly or chronic cases that its
progressive character is so well seen. Haygarth 7 men-
tions that 20 out of 34 cases had the hands affected first,
and Ord8 24 out of 38. Garrod out of 500 found that
252 commenced in the hands, 64 in the knees, and 28 in
the feet ; whilst in 430, or 86 per cent., the hands were
affected at the same period of the disease.
In the 78 cases I take for comparison, I could only get
a reliable history in 50 with regard to the joint first
affected. Out of these 50, 34 or 68 per cent, began in
the hands ; 8 or 16 per cent, in the ankles ; 5 or 10
per cent, in the knees ; 2 or 4 per cent, in the shoulders,
and neck ; and 1 or 2 per cent, in the elbows and hips.
The disease rarely, or never, travels down a limb,
although it may occasionally do so from a knee or elbow
to the fingers or toes. It is noticed that the joints
most liable to other conditions, are those most liable to
be affected also in this complaint, with one exception.
This is the temporo-maxillary joint, which is rarely
affected in other disorders, but shows a peculiar liability,
almost pathognomonic, to be affected in rheumatoid
disease. It may happen that the disease in the jaws is so
extreme that all movement is prevented, and feeding has
to be effected through the vacant space left by the
Garrod' s
Percentage.
Percentage
hands affected..
97*4 .
.. 86-0
elbows ,,
84-6
.. 25-0
neck ,,
82-0
. —
knees ,,
73-0
60-6
ankles ,,
67-9 .
.. 34-4
jaws ,,
67-9 .
.. 25-0
shoulders ,,
61-9
.. 25-0
hips ,,
12-5 .
.. 14-6
sterno-claviculai
2-5
—
104 RHEUMATOID ARTHRITIS.
removal of a tooth. The inability to open the jaw may
only be from stiffness and cicatricial contraction, but it
may also happen from true ankylosis.
Garrod gives a table of the joints most frequently
affected. For comparison, I also give my results : —
66
64
56
53
53
48
10
2
The centripetal order is broken at the neck, and knees,
but as these joints are specially liable to arthritic trouble
we would almost expect them to be so also in this disease.
In acute rheumatism, the knees are the joints most
frequently affected. One of the most marked features of
the disorder is its symmetry. This is not only seen with
regard to the joints affected, but also to the time of the
invasion, and, to a less extent, to the degree of severity
with which individual joints are affected. It is usual to
find one limb more affected than the other, and the peri-
pheral joints more than the more central ones. This is
often beautifully demonstrated. Garrod says this sym-
metry is carried so far that corresponding portions of
the cartilages are destroyed. This I cannot confirm.
When ankylosis occurs it may be from true, or fibrous
ankylosis, or more rarely from interlockings of the
osteophytic out-growths. This latter is most common
in the case of the jaws. Fibrous ankylosis may usually
be diagnosed from true or bony ankylosis, by some slight
movement detected on careful examination, or the attempt
to obtain movement may cause a contraction of the
muscles which oppose it, or else pain may be induced.
SYMPTOMS. 105
Spondylitis, or disease of the vertebrae, is not uncommon,
but it is confined almost entirely to the acute form.
In all cases, at one time or another, there is pain. The
pain is varied, and arises from many different causes.
That arising in the joints is, as a rule, of a gnawing
character, is made worse by movement, and often by the
warmth of the bed. It differs in intensity, in different
cases, and from time to time. Although there may be
no actual pain in the joints, patients often complain of a
pain as if the joints were being stretched, in the liga-
ments, and tendons. Pain is usually less in the joints
distended with fluid, but in acute cases with comparatively
no effusion, and where the cartilages rub one on another,
it is most marked. Besides this we may have pain from
cramp or spasms of the muscles, or there may be pain
referable to the bones. Again, we have neuralgic pains ;
and pain along the course of a nerve, due to neuritis.
In some cases there may be radiating pains which, if
there be spondylitis, is probably due to irritation or
compression of the nerve roots.
We must now consider the deformities and dislocations
which ensue. In every joint affection there is a
certain amount of deformity or distortion due to the
thickening and swelling of the joint tissues. Possibly in
rheumatoid arthritis it may stop at this stage, but, on the
other hand, as it progresses, and as the tissues become
contracted, destroyed, or greatly weakened, there may
arise those great alterations from the normal which
cause so much crippling and distortion. The disease, as
it advances, may cause an increased tonicity on the part
of certain muscles, and a weakness, or atony, on the part
of others, the result being a deformity which, although
at first readily reducible, soon becomes irreducible and
permanent. Along with the development of such
deformities we find marked wasting, and shortening of
106 RHEUMATOID ARTHRITIS.
certain muscles which may occur to such an extent that
joints quite free from disease may actually become partially
or completely dislocated, as has also been known to occur
in such diseases as paralysis agitans, congenital brain
atrophy, etc. (Plate VIII, Fig. A).
This process is of course very slow, and chronic in its
course. A somewhat similar condition has been described
by Jaccoud,9 as occurring in his " Kheumatisine fibreux."
Such deformities also occur in certain conditions of the
nervous system, and in all chronic forms of arthritis.
In rheumatoid arthritis the principal deformities are
seen in the hands and knees. The deformities of the
hand occur in two ways. There may be deflection to
the ulnar or radial side, or there may be extension or
flexion. A combination of these two types is what we
most commonly see. Let us first study the deflection
type.
The disease having commenced in the fingers, spreads
in course of time to the knuckles and wrists. These be-
come large, and nodular, and, probably, at the same time
some deflection of the fingers occurs. This may either be
ulnar, when the whole of the finger is involved, or else
radial, when only the terminal phalangeal joint is affected.
This radial deflection of the terminal joint has been
explained, by some, as being due to osteophytic outgrowths
on the ulnar side. The ulnar deflection only takes place
from the knuckle joints, and, except for radial deflection
of the terminal joints, the deformity of the phalangeal
joints is usually confined to a fusiform enlargement
due to synovial thickening (see Plate VIII, Fig. B, and
Plate IX, Fig. A).
When, however, the knuckles have become affected the
fingers may begin to deflect from that joint, but always to
the ulnar side. At first easily reducible, it rapidly becomes
irreducible. These deformities are brought about prin-
PLATE VIII.
Fig. ..4.— Dislocation backwards of index finger through relaxation of
ligaments and erosion of the cartilages and head of the bones ; also partial
dislocation of ring finger.
Fig. B. Shows ulnar deflection
SYMPTOMS. 107
cipally and primarily by relaxation of the ligaments and
tendons. Herringham suggests that it may be caused by
atrophy of the abductor indicis, and by the then unsup-
ported ringer pushing the others to the ulnar side.
Duckworth11 points out that such atrophy is not a
constant feature, and this therefore has to be discounted.
Pure atrophy alone will not cause it.
As a rule the thumb escapes, if the terminal joints alone
are affected, but it suffers if the disease becomes more
general. As the wrist enlarges the natural shape of the
arm and forearm is lost, and it comes to appear as
if the limb from the elbow to the wrist were of the same
thickness. One often notices that the bursae in the neigh-
bourhood of the olecranon are enlarged, and it is fairly
common to find that cartilaginous bodies have developed
in these bursae. In the larger joints it is usually
impossible to find any deflection. The deformities
arise in a similar manner in the feet, but are less
common.
Under the second type we find those deformities due
to flexion or extension. They were first described and
classified by Charcot,12 who divided them into two main
types, with several sub- varieties :—
I. — The first form is that most often met with. It is
marked by
(a,) Flexion of the terminal phalanges on the second
at an obtuse, right, or even an acute angle.
(b,) Extension of the second phalanges on the first.
(c,) Flexion of the first phalanges on the metacarpals.
(d,) Flexion to a less obtuse angle, of the metacarpals,
and carpals on the bones of the forearm.
(e,) In a great many cases, inclination of all the fingers
to the ulnar border of the hand.
The sub-varieties are : —
(a,) The first and second phalanges being in the same
10S RHEUMATOID ARTHRITIS.
axis, form a single column, with the other characters as
the main type.
(b,) The terminal phalanges are extended on the second,
and the backs of the fingers appear excavated beyond the
prominent heads of the metacarpal bones.
II. — The second type is characterised by
(a,) Extension of the terminals on the second phalanges.
(b,) Flexion of the second on the first phalanges.
(c,) Extension of the first phalanges on the metacarpals.
(d,) More or less marked flexion of the carpals on the
bones of the forearm.
(e,) In some cases deviation of all the fingers towards
the ulnar border of the hand.
The sub-varieties are : —
(a,) Flexion of all the segments of the hand, except the
terminals, on one another, so as to appear rolled up.
(b,) Is similar, except that there is extension of the
second on the first as well.
With regard to the thumb, it is usually flexed, but
occasionally it is found extended. Combined with these
changes there is usually flexion of the elbows, pronation
of the forearm, rigidity of the shoulder, and the upper
limb is fixed on the chest. Garrod makes the flexion or
extension of the middle joints the basis of his classification,
and which, therefore, necessitates the inclusion of the
second sub-variety of the flexion type as a sub-variety of
the extension type.
With regard to the lower limbs the hips usually remain
mobile, but the knees are flexed and fixed.
Charcot says that the chief deformities are as follows : —
(a,) The lower end of the femur projects in front of
the head of the tibia ;
(b,) The internal condyle becomes less prominent ;
(c,) The patella, thrown outwards, rests on the outer
condyle ;
SYMPTOMS. 109
(d,) The head of the fibula projects externally.
In the tibio-tarsal joint ankylosis is common. The
foot is, as a rule, abducted, and rests on its inner edge.
The big toe is turned outwards, so as to cover the other
toes. With regard to the cervical vertebrae one often
sees the head thrown forwards, and bent on the sternum,
so as almost to let the chin touch it. The neck is
widened posteriorly.
If we now turn to the deformities of the knee joints,
we see that the joint is almost invariably flexed, and
mayhap slightly rotated. Can we account for this in
any way '? In disease of the condyles of the femur we
know the leg always assumes a flexed position to a
greater or less extent, and that after flexion, the foot
rotates out, and rotation increases the flexion. In
diseases of the synovial sac, 'unattended by disease of the
condyles, cartilages, lateral or crucial ligaments, the
entire joint remains straight.
In diseases of the entire joint, including the cartilages,
the leg always flexes, whether there is fluid present or
not.
I must qualify these propositions by saying that certain
pathological changes, which may have taken place, may
modify these deformities. But such exceptional de-
formities are always easily accounted for, as, for instance,
that seen in Charcot's disease, or in cases attended by
complete destruction of either condyle or either side of
the tibia.
Many experimenters have tried to account for flexion
upon the fluid hypothesis. It is true that when the knee
joint is forcibly injected it will flex slightly, to give the
greatest possible capacity to the capsule, but this is in-
sufficient to explain the deformities.
The fluid hypothesis is wrong, because in, by far, the
largest percentage of cases, there is no liuid effusion, and
no RHEUMATOID ARTHRITIS.
large serous effusions are often unaccompanied by flexion,
and after a joint is evacuated in large effusions it does
not resume the straight position. These are valid
reasons why the fluid hypothesis is incorrect. Let us
now examine a knee-joint.
It is a hinge which, when in the straight position, is
firmly fixed, owing to the tension of the lateral and
crucial ligaments. This forces the articular surfaces
firmly together and prevents lateral motion. The leg
flexed, there is lateral motion of the joint, which increases
as the leg flexes, and not only lateral but rotary motion.
The is due to the relaxation of the crucial and lateral
ligaments by flexion. Another fact : the patella, and a
portion of the capsule anteriorly receive their nerve-
supply from the obturator, and probably from the an-
terior crural. The other portion of the joint is supplied
from the great sciatic. The great sciatic supplies the
flexor group, while the obturator and anterior crural
supply the extensor group. A clinical fact is, that when
the entire joint is attacked with acute inflammation, all
the muscles surrounding it are affected by spasm. Still
flexion rapidly takes place, whereas disease of the con-
dyles always produces great spasm and rapid atrophy
of the flexors, while the extensors remain quiescent.
Diseases limited to the patella produce spasm and
atrophy of the quadriceps extensor femoris.
In rheumatoid arthritis, however, we find certain
muscles presenting a weakness (usually to extension),
resulting from an atrophic condition, and others (usually
the flexors) a condition of increased tonicity. The result
is naturally flexion, and, as the limb flexes, rotation
follows, and we have the deformity so commonly seen.
The increased tonicity arises probably by reflex irritation
from the joint.
The question has been raised, How do deformities, as a
SYMPTOMS. in
whole, arise ? Some have held that they arose from an
intentional desire to lessen the pain. Trastour,13 and
Beau,14 were both of this opinion. Charcot held that
they were due entirely to muscular contraction, spasmo-
dic if not convulsive. These spasms are caused according
to him by a reflex action due to irritation in the joints.
This view was also taken by Crocq. Nowadays it is
recognised that they arise from the weakness of one set
of muscles being more than overcome by the strength of
another set. In the lower leg and foot we may instance
the long flexors, extensors, and interossei as being
specially affected. These latter flex the first row of
phalanges, and extend the second, thus accounting for
many of the deformities. When they are strong we will
have deformities of the extensor type, and, if weak, of the
flexor. It must not be forgotten, however, that there
are accessory causes. The weight of the limbs, and the
more or less decided laxity of the ligaments, all help in the
production. Such deformities are not exclusively the
property of rheumatoid arthritis (and in fact are not so
very common in it), but may occur in gout, chronic
rheumatic arthritis, paralysis agitans, etc.
Dislocations. — We find that dislocations either partial
or complete arise from the lengthening of certain liga-
ments, due to a softening or erosive process, combined
with increased tonicity of certain muscles ; whilst the
opposing ones have undergone atony, or else from the
ulceration of the heads of the bones.
We find that the most common dislocations are those
of the knees, wrists, hips (in old people), and fingers.
In the case of the knee, the tibia is most often dislocated
backwards, the wrist either backwards or forewards, and
the fingers on to the palmar aspect, the distal bones
being displaced under the proximal ones through the
anterior ligaments giving way (see Plate VII, Fig. A).
ii2 RHEUMATOID ARTHRITIS.
In chronic cases, we find the deformities much more
marked than in the acute, and dislocations are also more
common. The most usual type for it to assume is dis-
location of the wrist and fingers forewards. As a rule
these dislocations and deformities become more pro-
nounced as the disease becomes more chronic, and
contraction of cicatricial tissue takes place. In cases,
chronic from the first, they are less pronounced, partly
owing to the osteophytic growths. It has been noticed
that a hand which is used, up to the last, does not
develop such a regular type of deformity as another,
which has been kept at rest.
2. Symptoms due to the presence of the bacilli in the
blood.
(a,) Cardiac conditions. — I must now touch on a much
vexed question, namely, the occurrence of cardiac lesions
during the course of the disease. Personally, I am of the
opinion that endocarditis and pericarditis, especially the
former, are much more common complications than one
would expect. The former is fairly often seen, but the
latter much more rarely (in only about 4-5 per cent.).
Charcot says that they occur pretty frequently, and pre-
sent the same characters as are seen in acute rheumatism.
They are usually seen in the acute stages or during an
exacerbation. To him they appear to be less grave than
those of acute rheumatism. He gives instances of these
lesions being found post-mortem. Bomberg,15 Todd,10
Trastour,17 Beau,18 and Ball,19 all mention cases in which
they have found cardiac lesion with rheumatoid disease.
Besnier20 supports this view also, but declares that
they are rare. Sir A. Garrod 21 does not believe that
they ever occur, and Dr. A. E. Garrod supports him,
although admitting that cases are seen with cardiac
lesion, due, he thinks, to some previous rheumatic
condition.
SYMPTOMS. 113
Out of 78 cases, I found 14, or 17*9 per cent., suffered
from cardiac conditions which had developed since the
onset of the rheumatoid attack.
In several others there were cardiac conditions, but
the history in these cases not being perfectly clear they
were ignored. I have had several cases under rny care
in which undoubted acute endocarditis and pericarditis
have developed during the period they were under
observation. Given a micro-organism circulating in the
blood, it is of course probable that we will have symptoms
referable to their growth on the endocardium and
pericardium. As I have said, the cardiac lesions, except
in the case of the pericardium, are seldom of a very
extensive nature, and, in the majority of cases, I have
found the mitral valve to be the one most likely to be
affected — the other valves less often. Clinically they
have no special characteristics.
(&,) Changes in the glands, etc. — In a considerable num-
ber of cases we find enlargement of certain glands, most
commonly those in the groins and armpits. In a few
rare cases I have found a chain of glands running up
from an affected joint. They invariably are found on
the proximal side of an affected joint.
I have never, as yet, found an enlarged spleen. The
glands are usually enlarged in size, from that of a hazel
nut, up to that of a walnut, and are painful on pressure,
the pain shooting up and down the limb, but otherwise
give rise to no symptoms.
(c,) Fibroid nodules and fibrinous exudations occur in
rheumatoid disease as well as in rheumatism, syphilis,
etc. The former are seen chiefly in adults, are chronic
in nature, are often painful and tender, and vary much
in size and shape. They are found in the subcutaneous
tissues, and often close to a joint. Their occurrence has
been noted by Howard,22 Payne,23 Duckworth,24 Pitt,25
8
ii4 RHEUMATOID ARTHRITIS.
etc. If we bold that these nodules consist of a central
necrotic area, surrounded by dense connective tissue and
cell exudation, there can be only one possible explanation.
The bacilli circulating in the blood must have caused an
endarteritis, with cell exudation and inflammation, which,
if the irritation be severe, has ended in a local necrosis.
Extensive fibrinous exudation giving rise to a hide-
bound condition of the skin has been noted by Jaccoud
and Pitt. The exudation in these cases much resembles
granulation tissue.
C— Secondary symptoms, op those due to the absorption
of the bacterial poisons.
1. Of these secondary symptoms, the principal may
be referred to the muscular system. In all acute cases
we have a certain amount of muscular atrophy develop-
ing sooner or later. It is one of the earliest and most
persistent of symptoms, but may vary greatly in degree.
In some it is so slight as almost to be imperceptible,
whereas in others the joint trouble seems quite secondary
to that of the muscles affected. One of its peculiarities is
selection of the muscles. It is noticed, as a rule, that
the extensors and interossei are peculiarly liable to be
affected, but not invariably so. One muscle only
or a whole set of muscles may be affected, and yet the
form and extent of the disease in the joints would
appear to have little effect on this phenomenon of
selection. It is this selection, and the increase of the
tendon reflexes, which prove that the changes are not,
entirely due to disuse. For we must remember that
prolonged disuse will give rise to an arthritis, combined
with muscular atrophy, having many of the symptoms
of a rheumatoidal one. Such cases have been mentioned
by Bonnet,26 and Tessier.27 The selective character of
the atrophy, in rheumatoid disease, is peculiar, and this
we see when we compare it with what occurs in alcoholic
SYMPTOMS. 115
muscular atrophy, where the extensors chiefly are
affected, especially of the legs ; with lead, where it is the
extensors of the fingers and wrist; and with diphtheria,
where it is the muscles of the throat, and internal
muscles of the eye that suffer most. It is still more
remarkable that the selective power of toxic agents
should exert itself on the motor filaments only, and not
on the sensory ones, or on them both together. Indeed,
in some cases, there is good ground for supposing that
even the trophic, and vaso-motor nerves may be specially
picked out. With regard to this point, we must bear in
mind that in these diseases, we have to do with a
peripheral neuritis, but in rheumatoid arthritis, it is
probably a central disturbance which is responsible. The
reflexes vary in different cases, but in a pure case of
rheumatoid they are usually slightly increased. This
would rather point to some irritative lesion somewhere. It
is possible that the slight changes seen in the reaction
of degeneration indicate a difference between an intoxi-
cation, and a degeneration. I am inclined to think so.
In the cases where the reflexes are absent it is almost
certain that we have to do with a neuritis, probably set
up by the joint inflammation or by toxines, or it maybe due
to descending degeneration. In the case of a neuritis,
there will probably be pain along the course of the
affected nerve and there will also be other characteristic
signs. The atrophy, as we see it clinically, has been said
to be of different kinds : (a,) either due to a neuritis
arising as is stated above ; but (b,) more commonly it is
attributed to some reflex nerve influence having its origin
in the peripheral nerves of the affected joints ; and (c,)
since the discovery of the micro-organism, I hope it will
be generally conceded that it arises, more probably from
some toxic nutritional condition of the ganglion cells of the
anterior cornua of the spinal cord. With regard to this
1 1 6 RHE UMA TOW AR THR1TIS.
question Gowers28 points out that the atrophy from disuse
is trifling, and tardy, and affects the muscles of the diseased
limb as a whole ; and that the whole limb being affected,
precludes the possibility of the atrophy being due to any
local inflammatory change. He further points out that
the changes are such as frequently result from degenera-
tive changes in the pyramidal tracts, due to changes in the
terminations of the pyramidal fibres in the gray matter.
As a further proof that it does not arise from a local
change is the fact that the whole of a muscle is affected,
and not only that part immediately in contact with, or
distal to, the affected joint. To cause this atrophy by
peripheral means, the irritation must be intense; but I
would much rather believe that it is caused by a local
agent circulating in the blood, such as a toxine affecting
the afore-mentioned centre. The atrophy resembles that
occurring in other forms of arthritic muscular atrophy,
not only in its distribution, with its increased myotatic
irritability, but also in the absence of any reaction of de-
generation. Should any neuritis have occurred, of course
we will get the reaction of degeneration. Fibrillary
twitchings have been occasionally observed in the wasted
muscles. A tendency to spasm occurs with the increased
myotatic irritability. This spasm may exist for hours,
and give rise to the most acute pain, usually having a
cramp-like character. Ballet 29 mentions cases accom-
panied by chronic spasm which occurred paroxysmally.
2. Symptoms due to changes in the circulatory
system.
The circulatory symptoms are various, and some of
them I will consider under the nervous system.
(a,) Fever. — The general body temperature seldom
shows much rise, but in the acute stages there is always
fever, usually of an irregular type. It seldom is high,
but, on one occasion, I have seen it as high as 105° Falu
SYMPTOMS. 117
That it rises nightly during the more progressive stages,
I have no doubt, but owing to its irregularity, and from
the fact that it is seldom high it is usually overlooked.
One reason assigned for the want of fever is that owing
to the condensation of the joint tissues the absorption of
the toxines is very slow, and no great quantity is ab-
sorbed at once. This, I think, is hardly a sufficient
explanation. Most of my hospital cases, where accurate
observations are taken, present a certain rise every
evening of from one to four degrees, and this may go on
for months, as a rule, quite unsuspected both by the
patient and by the medical attendant, unless attention
be specially drawn to it.
Amongst the other symptoms we have (b,) Tachycardia
or increase of the heart rate. Sir Dyce Duckworth first
pointed out that palpitation in this disease was not un-
common. An increase in the pulse rate was also pointed
out by Charcot,30 but it was probably not until Spender 31
drew attention to it, that any special significance was
placed on this. Spender says, that in the acute cases,
the greater number are characterised, from the beginning,
by an increased velocity and tension of the heart's action,
and the pulse may go up at once to between 80 and 90,
and remain so for years. He says, "we are startled by
counting a steady pulse of much tension, varying from
90 to 110 The pulse quickens synchronously
with the earliest sign of osteo-arthritis ; there is a gradual
rise until the numerical frequency of 110, 115, or 120 is
reached, and there is scarcely any physiological variation
during day or night the body is absolutely
non-pyrexial, and the icy purple coldness of the hands is
often a striking fact. There is no ha^mic murmur, and
there are no signs of the heart being in any way affected.
The acceleration of the circulation is not paroxysmal,
the phenomenon does not belong to that group lately
n8 RHEUMATOID ARTHRITIS.
described by Dr. Bristowe,32 in which the rate of pulsa-
tion now and then suddenly increases, and as suddenly
lessens, nor is there any sign of venous engorgement or
of local oedema. It is as if the heart were running along
without check ; as if the inhibitory power of the pneu-
mogastric nerve were partially withdrawn, or partially
neutralised by a cerebral influence which cannot at
present be denned." Such, in his own words, is the
condition which he describes. I am afraid, I cannot
altogether support him in his observation. It is un-
doubted that we all see cases of rheumatoid arthritis
with an increased pulse rate, but cannot this be accounted
for by the fact that in most cases there is some pyrexia,
and by the fact that most hearts in rheumatoid disease are
undoubtedly neurotic. Sit down quietly by the patient's
bedside, and you will find that a pulse, going at the rate
of 120, or over, will gradually subside and diminish in
frequency. Such at least has been my experience in a
certain proportion of cases. But, now and then, we
undoubtedly come across cases corresponding in all
essentials to those described by Dr. Spender. They are
however, not very common. The tachycardia probably
arises from the cardiac nerves and centres having come
under the same influences which affect so many of the
other portions of the nerve system.
We now turn to another class in which (c,) Ansemia
occurs. Although resembling many other anaemias
in being secondary and symptomatic in nature rather
than primary or idiopathic, that of rheumatoid arthritis
is none the less interesting ; and in its details may be
classed with those forms seen in various other infective
diseases. We seldom find it very marked except in
advanced and very acute cases, but in all, even the
slightest, there is, as a rule, a certain amount of blood
deficiency. Boughly speaking in about 95 per cent, of
PLATE IX.
Fig. A. Shows fusiform deformity of index finger.
Fig. B. — Haemorrhage under nails in Rheumatoid Arthritis.
SYMPTOMS. 119
the cases presenting themselves, in all stages, do we
find it to a greater or lesser degree. We rarely find
extreme pallor of the skin, the patients presenting more
often a sallow or brownish yellow complexion, with
moderate blanching of the mucous membranes. This
sallowness may, by degrees, pass into deeper shades,
until it insensibly merges into a distinct discolouration.
Not infrequently it is accompanied by functional cardiac
bruits and venous hums. Haemorrhages, so common in
other anaemias, are rare, but not unknown. They are
very rare from the mucous membranes, being most
commonly seen as small purpuric spots on the legs. I
have seen it two or three times as hsematemesis and
haemoptysis, and once under the nails of the fingers and
toes. Of course haemorrhages are rare, as they mostly
occur in cases where there is 50 per cent, or more blood
deficiency and where it depends more on a diminution of
the corpuscles than on that of the haemoglobin.
(d,) Haemorrhages. — Purpuric haemorrhages are usually
small and are usually subcutaneous. They almost never
occur from the mucous and synovial membranes. Haema-
temesis I have seen several times, and haemoptysis
once.
In the course of a year, I have on an average, seen
perhaps six or eight cases where purpura was well
marked, the haemorrhagic effusions usually occurring
on the front of the legs, and, more rarely on the forearms.
A very interesting case was one where it had occurred
under the nails of both hands and feet, before admission.
When first seen it was beginning to clear up, but showed
as a brownish discolouration under the nails. The ac-
companying photograph (Plate IX, Fig. B), shows
the lesion well during the process of clearing up. The
haemorrhages are almost undoubtedly due to the
rheumatoidal toxic poison which induces anaemia with
1 20 RHE UMA TOW A R THRIT1S.
dilatation of the blood-vessels and extravasation of their
contents.
3. Symptoms due to abnormalities of the nervous
system. Now, although strictly speaking almost all, if not
all, the secondary symptoms are due to derangement of
the nervous system, yet I have chosen for obvious reasons,
to describe them separately under the various systems
in which they occur, leaving only neuritis and the more
miscellaneous trophic changes to be considered under this
heading.
(a,) Neuritis is a fairly common complication, and
usually arises from inflammation spreading from the
joint to the nerves in the proximity, more rarely from the
effect of the toxines on the nerves themselves. Its most
prominent symptom is pain along the course of the nerve,
with atrophy of one or more muscles. This may become
extreme. Faradic irritability is lost, but that to voltaism is
increased in amount and often, but not always, altered in
quality. In slight cases the increase of voltaic irritability
may be trifling. In the nerves the irritability to both
currents lessens and is ultimately lost. There is a
tendency for it to spread to other branches, and nerves,
and to gradually affect nearly all the muscles of a limb.
Muscle -reflex action (myotatic irritability) is invariably
lost. The muscles iri these cases are paler than normal
and smaller m bulk. The fibres are reduced in size, and
are pale in colour ; the transverse striation may be pre-
served or they may be granular ; and the nuclei of their
sheaths, and interstitial tissue may be increased in
number. These cases differ much from the ordinary
cases of rheumatoid arthritis, and often give rise to
difficulty in arriving at a diagnosis.
Apart from the direct spread of inflammation from the
joints to the nerves, the neuritis may be caused by the
poison generated by the micro-organisms. Recent re-
SYMPTOMS. 121
searches suggest that it is these poisons, and not the
organisms themselves that act on the nerves. The fact
of symmetry helps to prove that it is a cause acting-
through the blood, and the selective action as seen is
also typical of the action of toxic agents upon various
parts of the nervous system.
(b,) Other trophic phenomena. — We best see, that some
disturbance of the trophic function of the nerves has
taken place, from the symptoms due to vaso-motor
disturbance. It is probably due to this that we have
those cold clammy blue hands, evidently a local asphyxia,
with sweating of the palms, pigmentation, etc. Along
with these, but more rarely, we see local erythema and
congestion. Occasionally distinct areas of atrophy of the
skin have been observed ; perhaps one of the most marked
and most common forms being that known as " glossy
skin." This condition was first described by Paget, and
more recently by Mitchell. The skin, in this condition,
looks as if it had been varnished, and much resembles
chilblains on a big scale, or else a highly polished scar.
The hairs for the most part disappear. The affected skin
is smooth, hairless, almost devoid of wrinkles, pink in
colour, and glossy. In contra-distinction to this we often
see a recent growth of downy hair, especially on the fore-
arms. Again, we may see a condition of scleroderma.
In this condition we have patches of skin white, and
ivory-like, indurated, and stiffened, and as if frozen.
The skin may be bound down to the tissues underneath,
and may impede movement, and cause deformity ; the
papillae of the skin being flattened, the cutis thinner than
usual, and composed of more homogeneous connective
tissue, and the skin as a whole is less fibrous than in
the normal. The hairs gradually disappear until a con-
dition of alopecia is observed. Along with this atrophic
condition a certain amount of chronic inflammation is
122 RHEUMATOID ARTHRITIS.
seen, as evidenced by the abundant nuclei in the altered
skin, principally around the vessels, and sebaceous glands,
and in the rete Malpighii. (Edenia of the subcutaneous
tissues, especially of the legs, has been observed by
Vidal, 33 and Charcot 34 unaccompanied, however, by any
cause which would ordinarily give rise to it. The nails
may become brittle, and deeply ridged in the longitudinal
directions. Hadden 35 has described ulcerations of the
fingers, and wasting of the soft parts is pretty common.
Fagge 36 mentions cases in which fibrous nodules occurred
some distance away from the diseased joints, as in the
muscles of the arms and forearms. They must be dis-
tinguished from ordinary rheumatic nodules. Colombel 37
also mentions various trophic changes, especially of the
skin.
4. Abnormalities of the integumentary system.
(«,) Increase in the ehromatogenous functions of the
skin. Dr. Spender 3S first drew attention to this
phenomenon. The pigmentation varies from light yellow
to a deep bronze colour, and it may occur in small
freckles, or in large blotches. It is most usually seen
on the forehead, temples, eyelids, hands, forearms, or
front of the legs. The freckles are round as a rule,
sharply defined from the neighbouring skin, are not
raised, but have a tendency to symmetry. When they
occur as blotches they are darker in colour, and are not so
symmetrical, except on the face, where they often sur-
round the eyes, involving the eyelids and spreading out
on to the forehead. The onset and clearing up of these
pigmentations can often be watched if the patient be kept
under careful surveillance for some period of time, and
are of use as giving some indication of the patient's
condition.
(b,) Sweating. — In most cases at one time or another
we see abnormal sweating. It may be a mere dampness,
SYMPTOMS. 123
or else it may be so excessive as to make the skin wring-
ing wet. It may be limited to one portion of the body,
such as the palms of the hands, soles of the feet, face, or
forehead, or it may be general. Although dripping with
perspiration, yet the patient's skin feels cold, and almost
deathlike, and they always complain of coldness of
the extremities. These are blue or of an unnatural
whiteness.
5.— The symptoms referable to the alimentary traet are
probably of less significance and are more of the nature
of a complication than those of the other systems, but
still in the large proportion of cases we find some alimen-
tary derangement. This usually takes the form of gastric
disturbance, accompanied by flatulence, and acid eructa-
tions. The bowels are almost always confined, and there
is sometimes a tendency to vomiting. The importance
of these disorders is appreciated when we know that
most of our treatment now-a-days is directed to improv-
ing the patient's general health, and to assist in the
elimination of toxic products, a thing we cannot do if
the digestive arrangements are out of order. It is also
of importance to remember that this may be the route
through which the micro-organism gains its access to
the system generally.
The urine is as a rule normal, but in some cases, Money39
found excess of urea and uric acid, and occasionally
transitory glycosuria. This excess of uric acid is denied by
most authors, and I have never found it. Drachmann 40
noted a diminution of the phosphates excreted ; Bocker
found a diminution of phosphate of calcium in the urine,
but there was four times as much found in the blood.
Apart from the cardiac conditions the principal visceral
complications are due to the occurrence of such diseases
as pneumonia, bronchitis, phthisis, interstitial nephritis,
etc. Sclerotitis, iritis, and conjunctivitis occasionally
1 24 RHE UMA TOW AR THRITIS.
occur. Deafness due to the ossicles of the ear being
affected, and aphonia, due to the implication of the
arytenoid cartilages, sometimes are seen. Certain skin
affections, apart from those already mentioned, such
as psoriasis, have been described as occurring in rheuma-
toid arthritis, but their presence is probably nothing
more than an accidental occurrence.
II. — Prognosis.
With regard to prognosis little can be said of an en-
couraging nature, if we look forward to a perfect cure.
Once a joint is destroyed, as it rapidly is, we can never
make it as of old. Cases seen early may be completely
cured, but once destruction of the cartilages has occurred
I see no possibility of this occurring. One can subdue
the acute stages, but still we have left the hardening,
and thickening, the pain, stiffness, difficulty of move-
ment, and a certain amount of crippling. Still it
is marvellous what can be done, and I would never say
that any case is absolutely hopeless, for by care and
proper treatment the pain can be alleviated, and life
made more bearable both to the patients themselves and
their immediate companions. At the worst, the com-
plaint is rarely fatal to life ; but what is life if one is a
total cripple, a trial to one's self and to all about one ?
On the whole I would say that the hope, to make the
joint, or joints, as good as they originally were, is futile —
it cannot be done, but we can relieve pain, subdue the
destructive elements, and leave only the actual joint
changes to be combatted. These are no small mercies,
and, in the near future, we may hope for even greater
successes. One warning I would give, and, it is, take
the disease in time, take it in its earlier stages, and you
will reap an adequate reward in the relief you have
obtained for the sufferer, and in the knowledge that
PROGNOSIS. 125
you have subdued what has hitherto been regarded as
an altogether incurable complaint.
REFERENCES.
1. Howard.— " Pepper's Syst. of Pract. Med.," 1885, vol. ii.,
p. 88.
2. Horaolle.— " Diet, de Med. et Chir. Prat.," 1882.
3. Garrod. — " Rheumatism and Rheumatoid Arthritis."
4. Spender.—" Osteo- Arthritis," 1889.
5. Baker, Morant.— " St. Earth. Hosp. Rep.," 1885, xxi.
6. Charcot.— " These de Paris," 1853.
7. Haygarth.— " On Nodosity of the Joints," 1805.
8. Ord.— " Trans. Clin. Soc.," 1879, xiii., and " Brit. Med.
Journal," 1884, vol. ii.
9. Jaccoud.— " Lecons de Clin. Med.," 1867, lecon xxiii.
Ii. Duckworth.—" Treatise on Gout," 1889.
12. Charcot. — " GEuvres Completes."
13. Trastour.— " These de Paris," 1855.
14. Beau. — " Gazette des HGpitaux," 19th July, 1864.
15. Romberg. — " Klinische Ergebnisse," 1846, and "Klinische
Wahrnehmuugen," 1851.
16. Todd.—" On Gout and Rheumatism," 1843.
17. Trastour. — Loc. cit.
18. Beau. — Loc. cit.
19. Ball.—" On Rheumatisme Viceral," " These de Paris," 1866,
p. 121.
20. Besnier. — "Diet. Encyclop. des Sciences Med.," 1876.
21. Garrod, Sir A. — " Gout and Rheumatic Gout," 1876.
22. Howard. — "Pepper's System of Medicine."
23. Payne.— "Brit. Med. Journal," 1883, vol. i., p. 622.
24- Duckworth, Sir D.— " Clin. Trans.," vol. xvi., p. 52.
25. Pitt. — " Clin. Trans.," vol. xxvii., p. 54.
26. Bonnet. — " Traite de Maladies des Articulations."
27. Tessier. — " Memoirs sur les effets de l'immobilite longtemps
prolonge des Articulations."
28. Gowers. — " Diseases of the Nervous System," vol. i. p. 498.
29. Ballet. — Quoted Garrod, loc. cit., p. 256.
30. Charcot. — Loc. cit.
31. Spender. — Loc. cit.
32. Bristowe.— " Brain," vol. x., 1888.
33. Vidal.— " These Inaugural," 1855.
34. Charcot.- -Loc. cit.
35. Hadden.— "Trans. Med. Soc," New York, 18S6.
36. Fagge. — " Principles and Practice of Medicine," vol. ii.
37. Colombel.— " These de Paris," 1862.
38. Spender. — Loc. cit.
39. Money.—" Lancet," 1887, vol. ii., and " Brit. Med. Journal."
1888, vol. i.
40. Drackmann.— " Nordisht. Med. Arch.," 1873, vol. v., p. 1.
126
CHAPTER VI.
TREATMENT.
Preliminary considerations — Antitoxine — C auses — Diet — Cloth-
ing — - Exercise — -Drugs — Creasote — Guaiacol — Guaiacol Car-
bonate — Benzosol — Phenols — /3-Naphthol — Betol — Salol —
Action of Creasote— Hudeocl — Douglas Powell — Intestinal Anti-
septics— Iron — Arsenic — Iodides — Salicylates — Actaea Eace-
rnosa — Ichthyol — Hyoscyamus — Relief of pain — Dr. Spender's
treatment — Guaiacol externally — Carbolic Acid applications —
Electricity — Thermal treatment — Alkaline and Sulphur Waters
— Bath — Aachen — Action of Bath Waters — Bath treatment — Aix
treatment — Hot Air Baths — Sea Voyages— Extension — Excision
— Summary.
Until quite recently, certain forms of Rheumatoid Arthritis
have been regarded as not only quite incurable, but also
almost impossible to alleviate. So far from this being the
case, I believe all cases, if recognised early, are curable, and
if, in the later stages, not curable, yet the attack can be
arrested, and further damage prevented. When much
disorganisation of the tissues, soft and hard, of a joint
has already taken place we of course cannot renew them,
and make them as of old, but we can arrest its spread,
and we can alleviate suffering, and by improving the
general health, give greater ease, and comfort — in fact,
the activity of the disease being subdued we have only
the permanent destruction, and disorganisation left to
deal with. This has been brought about partly by our
better comprehension of the nature of the disease, and
partly by newer methods of treatment. Now that we
know it is a parasitic disease, our way becomes
clearer, and we have, at last, a definite aim in our
methods and modes of treatment. The discovery of
TREATMENT. 127
micro-organisms as a cause is too recent for us to have
yet found an antidote, but I am in hopes that before long
one, having as powerful an effect for good, as that of
diphtheria, will be found. Meanwhile, and, until it is
obtained, we have to content ourselves with some of the
newer drugs, with antiseptic properties ; and these in
conjunction with dietetic, and thermal treatment have
yielded such remarkable results that I consider the future
full of promise. I am speaking of pure cases of rheuma-
toid disease, and not of "Malum coxae senilis," a most
important fact to remember.
Before considering the treatment proper, it is of impor-
tance to bear in mind that one of the first considerations
which any medical man, called upon to treat this affec-
tion, must deal with, is the cause or lesion through which
the poison has gained access to the blood. In this
respect it differs from those diseases, of which diphtheria
is a type, in that, in them, the disease can be attacked
at the seat of inoculation; whereas, in intra-joint disease
the organism can only be sustained while it elaborates
its antitoxines, and marshals its leucocytes to do battle
with the invading legions of inimical micro-organisms.
During the course of treatment one must carefully guard
against anything likely to lower or debilitate the system.
The importance of this is understood, when we remem-
ber, that it is only when the general constitution is
lowered that the insidious onslaughts of micro-organisms
are likely to prove successful. And thus when we glance
at the causes which make patients liable to the disease, we
see what a great role debilitating agencies play, and how
it becomes of the utmost importance, by the most careful
scrutiny of the past, and of the family history, to check
those agencies before they can do further harm. By
such enquiries one is usually led to an offending organ
or function, and by the rectification of which, as far as
128 RHEUMATOID ARTHRITIS.
is possible, we not only improve the general health, but
may prevent farther infection.
We may now proceed to the consideration of the
principles of treatment, as we understand them,
dividing them into three sections : (I) Diet, clothing,
etc.; (II) Drugs; (III) Thermal, electric, and surgical
treatment.
I. — Diet, Clothing, etc.
(a) Diet. — No more fatal mistake can be made than to
place a patient on what is popularly known as "low diet."
This course was for years followed with disastrous results,
in consequence of the belief that the disease was to a
greater or lesser degree due to gout. Such we now know
not to be the case, and the diet must, as far as possible,
resemble that which one would recommend for that worst
of all wasting diseases, namely, phthisis. Of course,
where considerable febrile disturbance exists care must
be taken to give suitable liquid nourishment until the
febrile state has passed. With this proviso the diet
should be of a nourishing, as well as of a mixed character.
The practice of limiting the amount of nitrogenous food
is not beneficial — in fact as much nitrogenous food as can
be digested should be given — care being taken to correct
any functional derangement of the digestive organs.
Fats are an important item, and above all in this class
stands eod-liver oil which should be regarded not as a
medicine, but as a food, and should in conjunction with
maltine be given at the termination of every meal. Of
vegetables, Spanish onion, and celery are the best.
Stimulants should be ordered, but not more than will
stimulate the secretion of the gastric juice — malt liquors,
and good wines being preferred. Each individual
case must be treated by itself, and no hard and fast
rules can be laid down — the physician must exercise
TREATMENT. 129
his own discretion. A good diet list is the follow-
ing :—
May take Soups : Bouillon, mutton, chicken, oyster, turtle,
barley, rice, bean, pea.
Fish : All that agree— boiled, baked, stewed or broiled.
Meats : Beef, broiled or roast ; lamb, roast or broiled ; mutton,
roast or broiled ; poultry, roast or broiled ; game ; sweetbreads ;
predigested meats (beef peptonoids, sarco-peptones, peptonized
beef -tea, essences of beef, beef jelly, etc.).
Eggs raw (and with whiskey, milk or sherry, sweetened),
poached, boiled.
Fats and Oils : Mutton, beef, butter, olive oil, cod-liver oil.
Vegetables : Greens, lettuce, celery, spinach, asparagus, cresses,
cauliflowers, onions, tomatoes, green peas, beans, lentils, and
other leguminous vegetables ; rice, well cooked, sparingly ;
radishes ; potatoes, in their jackets, very sparingly.
Bread: Wheat and gluten bread, toast, milk toast. Bread
should be at least one day old, and only a small quantity should
be taken.
Fruits, Nuts, etc.: Oranges, lemons, pears, apricots, peaches,
grapes, fresh figs, and dates ; baked apples sparingly, and avoid
them raw ; walnuts, almonds, filberts, sparingly.
Drinks : Boiled water, Apollinaris and other carbonated waters,
hot milk, cream, milk punch, egg-nog ; peptonized milk, lemonade,
ginger ale, sherbet ; alcoholic drinks as prescribed (brandy, whis-
key, wines, and malt liquors) ; malt preparations ; coffee, cocoa,
chocolate, tea sparingly and weak.
It is important to take food often and at regular inter-
vals, care being taken that not more than three hours,
except during sleep, passes without food. A glass of
milk, or milk punch or liquid peptonoids, should be
placed within easy reach in case of waking during
the night.
During the day the following arrangements can be
followed : —
7.30 a.m., and while still in bed, patient should have a cup of
milk with a dessert spoonful of whiskey, brandy, or other stimulant,
or with a small quantity of tea, cocoa, and a small piece of bread,
toast, or biscuit.
8.30 — 9 a.m., breakfast of milk with a little tea, coffee or cocoa,
toast or bread and butter, bacon, ham, fish, or eggs.
9
130 RHEUMATOID ARTHRITIS.
11.0 a.m., a tumblerful of milk, a cup of broth or beef-tea, or a
sandwich, and a glass of wine.
1 — 1.30 p.m., a substantial meal of meat, poultry, fish, or game,
with fresh vegetables, some light pudding or cooked fruit, and a
glass of wine or malt liquor.
4 p.m., a glass of milk, with a small quantity of tea, coffee, or
cocoa, and some bread and butter or a plain biscuit.
7 p.m., another substantial meal similar to the mid-day one.
9.30 — 10 p.m., a cup of milk or bread and milk, or milk with
some farinaceous food, such as Nestle's, Mellin's, or Liebig's,
etc.
(b,) Clothing. — The body must be encased in light wool-
len garments, worn if possible next the skin, care being
taken not to over-clothe. A thin flannel vest and drawers
with a piece of wash-leather inserted inside the fabric,
next the skin, over the joints, is a most excellent plan.
The feet must be carefully guarded, especially in damp
weather. All- undue exposure to damp and cold, it is
needless to say, should be avoided, and the patient must
be warned, if possible, not to expose himself during east
and north-easterly winds.
(c,) Exercise. — During an acute attack, of course the
patient should be confined to bed. As a rule this is un-
necessary during the more chronic stages, a moderate
amount of exercise being of advantage. If not able to
walk, one should be careful to see that a sufficiency of
fresh air either by carriage-driving or in a Bath-chair is
obtained. The use of carefully regulated and graduated
gymnastics and special movements, passive exercises,
the use of pulleys, weights etc., are all of benefit.
II. — Dkugs.
Almost every drug in the Pharmacopoeia has at one time
or another been used in this most intractable complaint,
and all with more or less indifferent success. As these
all, one after the other, failed me, I turned to some of the
newer drugs whose properties as antiseptics and elimina-
TREATMENT. 131
tive agents appeared to promise success. After prolonged
trial and experimenting, my results and deductions have
led to the following facts being ascertained.
Treatment by drugs may be divided into three
classes : —
A.— Those substances which when administered internally
are antagonistic or antidotal to micro-organisms, or to
their products.
B.— Those substances (1) which act by improving the
general tone of the organism, and help it to resist the
inroads of micro-organisms ; and (2) those whose action
is more or less indefinite, and which have been given
empirically, and to relieve symptoms, and
C— Those substances which are of use when applied
externally.
A.— Those substances which are antagonistic or antidotal
to the micro-organisms or to their products.
In this group we have three sets of substances which
from their nature give promise of benefit in rheumatoid
arthritis. The drugs in each set enter into combination
with various organic acids, and the resulting substances
have all more or less direct antitoxic action. Their action
varies in strength and efficiency according to the nature
of their constituents. This is because their efficiency
depends on the rapidity of their decomposition after in-
gestion, and the rapidity of absorption after decomposi-
tion has occurred. Their primary action is undoubtedly
a direct local one, and they to a greater or lesser extent,
counteract bacteria, and their products. After absorp-
tion they act more as eliminative substances entering
into combination with the toxic albumens, thus favour-
ing their elimination. The longer the substance takes to
decompose the greater its local action, and, in inverse
ratio, the greater the rapidity of decomposition the greater
the rapidity of absorption and eliminative power.
i32 RHEUMATOID ARTHRITIS.
The three sets of substances I have tried and experi-
mented with are: —
1. The ereasotes or guaiaeols which enter into com-
bination with carbonic acid yielding guaiacol carbonate,
and with benzoic acid yielding benzosol.
2. The phenols which enter into combination with
salicylic acid yielding salol ; and
3. The naphthols which enter into combination with
salicylic acid yielding betol, and with benzoyl chloride
yielding benzonaphthol.
I have employed these drugs largely in the treatment
of this disease, and out of them all I have found a few of
real use ; the principal being those belonging to the
creasote group, probably from their quicker decomposition
and greater eliminative powers. Those belonging to the
naphthol group are practically un absorbed, and act almost
entirely locally. From my experience, I should say that
it is the bases in all cases which are of use, and not the
acids with which they combine. This is specially notice-
able with the salicylic acid combinations, which instead
of being the most useful, as one might fairly expect, are
the most useless. The following are of use : (1) Creasote ;
(2) Guaiacol ; (3) Guaiacol Carbonate ; (4) Benzosol ; (5)
/3-Naphthol; (6) Betol, and to a less extent, (7) Salol.
My conclusions may be briefly summarised. The
ereasotes would appear to have a more or less specific
action on the disease ; whilst the phenols, with the ex-
ception of salol, appear to be indifferent and useless ; but
the naphthols by their intestinal action apparently are
of much use, in a few cases. Salol and betol also act
as local antiseptics, but are less actively useful and their
eliminative powers appear to be feeble. Salicylic acid,
rarely is of use ; but in those cases in which salol
and betol act beneficially, salicylate of soda also does
well.
TREATMENT. 133
The question now comes to be, How do the creasotes
and their compounds act? It is supposed that they,
their compounds, and derivatives, have not more than
any other drug, any specific action on micro-organisms.
According to Hudeod x they act not as antibacillary
agents, but rather by setting up a substitutive irritation
which successfully opposes the microbic inflammation.
Dr. Douglas Powell2 says that although creasote has
little direct action, yet it has an indirect germicidal
function. Others have stated that they act on the
system generally, having no direct influence, by means
of the stomach or by improving the general nutrition.
They act locally, we know, on the alimentary canal
before absorption, and afterwards by favouring the elimi-
nation of the toxic albumens with which they combine.
Whilst in the gastro-intestinal tract they act on the
mucous membrane as well as on the intestinal contents.
As absorption proceeds their virtue as local antiseptics
diminishes. It has been proved impossible to sterilize
the blood, even after large doses (Hoelscher 3), so it is by
their secondary action that such drugs are more especially
valuable. This may be so, but has it not been too readily
assumed that these drugs have no direct action on the
micro-organisms themselves. May they not to a great
extent impair their power to grow and multiply if they
cannot actually destroy them ? One of the arguments in
favour of the disease being caused by micro-organisms
in the joints, is this fact, that creasote and its allies are
of use. Were the disease due to toxines, the phenols
and naphthols would probably be of greater service, as
they would be more likely to arrest their production,
toxines being mostly produced in lesions more open to
external influences, such as the intestinal tract, etc. It
has been proved that the best antiseptics for the stomach
are bismuth and charcoal ; for the small intestine, salol,
134 RHEUMATOID ARTHRITIS.
sodic salicylate or benzoate ; and for the larger bowel,
/3-naphthol and charcoal (Bates4). /3-naphthol has
proved of special value, as on it the patient's general
health has greatly improved, as well as the joint pains
and swellings. Salol and betol appear to be less active
than their bases, and they are not so remarkably useful
as to encourage me in their further use.
1.— The Creasotes.
The creasotes are the drugs par excellence for rheu-
matoid arthritis, and without which one would feel
helpless indeed, and one would drift back into that slough
of despond in which for years those, much in contact
with this disease, have been. Now, however, I hope a
new era is dawning, and that at last we see a ray of
light to lead us onward.
(a,) Creasote 5 10 u (pure beechwood creasote) may be
used in small doses, beginning with 2 drops and
gradually increasing the dose to 15 or 20 drops,
divided into three or four doses each. It may be given
made up with alcohol, with some flavouring material,
with cod-liver oil, or preferably in capsule. Creasote,
although a complex body, has for its largest constituent
guaiacol, and to whose agency it owes most of its efficiency.
It is strongly tasted, and has a most pungent odour.
It is liable to cause nausea, gastric irritation, and to take
away the appetite. Its use therefore is not unattended
with difficulties.
(b,) Guaiaeol 12 (OH. C6 H4. OC3), the principal consti-
tuent of creasote, has also a pungent taste, and smell, and
its administration is followed by the same drawbacks as
that of creasote. Since the discovery of some of its
compounds and derivatives, it has been less frequently
used, but the benefit derived from its use is undoubted.
It is best administered in capsules, or else dissolved in
some form of tincture, in daily doses of nixx and over,
TREATMENT. 135
and continued steadily for months. Should it not be
bearable by the mouth, it may be administered hypoder-
mically, as is recommended, in phthisis, by Dr. Picot,13
of Bordeaux, and others. Administered thus it acts by
reducing the temperature, causing a profuse sweating
and allaying pain. Sciatica and supra-orbital neuralgia
have been treated so with marked success by Anders.19a
He used n\ij of guaiacol in rn.x of chloroform. Cham-
ponniere 19b used 10 centigramme doses dissolved in
sterilized oil, and found it acted as a local anaesthetic
as well as an analgesic. I have not, as a rule, found this
hypodermic medication necessary. As an analgesic I
always obtained success when applied externally, and for
its other properties its compounds are as active, and are
so much more easily administered, and assimilated, when
given by the mouth.
(c,) Guaiacol Carbonate is an insoluble, tasteless, odour-
less, white crystalline powder. It has none of the
unpleasant effects of creasote or guaiacol which are so
liable to irritate the stomach, and to destroy the appetite.
It is slowly decomposed in the bowels, yielding guaiacol,
which is absorbed into the blood, and carbonic acid.
Within half to one hour after ingestion the guaiacol can
be traced in the urine. It is by far the most useful
of the whole series, but from its expense it has not been
used so generally in hospital practice as it might have
been. It is easily taken by the mouth either in powder,
in pill, or in cachet. It is the drug on which I
place most reliance, and in few cases have I found
it ultimately to fail. It has now come to be my routine
treatment, and I employ it in all cases, where active
disease exists, in doses of grs. v — x, repeated three to
four times daily. In no case have I seen any symptom
of intolerance, nor have I noticed any evil effects
produced.
136 RHEUMATOID ARTHRITIS.
(d,) Benzosol (Benzoyl-Guaiacol C14 H12 03) is a taste-
less, and odourless body which splits into guaiacol,
and benzoic acid in the digestive tract. It was introduced
for use in phthisis by Dr. Walzer. It is insoluble in
water, but is so in the gastro-intestinal tract, slightly in
the stomach, but principally in the small intestines. It
is very little soluble in glacial acetic acid, but is soluble
in chloroform, ether, and hot alcohol. The dose is grs. vj,
repeated three or four times a day. It is also of much
use, but appears to be slightly less active than the
carbonate.
Owing to the nauseous taste, disagreeable eructations,
and gastric irritation set up by creasote and guaiacol,
they are now seldom used internally. More often we
use guaiacol carbonate and benzosol. The effect of any
one of the group is to improve the appetite, relieve pain,
lower the temperature, stop all inflammatory process,
and to improve the joint conditions. The patient sleeps
better, gains flesh, pigmentation, and other vaso-motor
anomalies improve, the hands are no longer cold and
dripping with perspiration, and the patient can move
about with a great deal less pain, and more comfort.
The general appearance also undergoes change, they are
no longer anasruic, anxious, and full of fancies, but say
and look as if they were on the road to recovery. Of
course such results are not obtained in a day, and are
only brought about by the most careful combination of
drugging and thermal treatment. With regard to the
drugs, benzosol is often more immediately followed by
relief of pain ; but for long continued and severe cases,
the carbonate is the more to be relied upon.
2.— The Phenols.
Salol is practically the only drug of this class which I
have found of use, and it only rarely. In a few instances,
combined with salicylate of quinine, the results have
TREATMENT. 137
been good, especially in cases complicated by intestinal
trouble. It is a valuable alternative drug, but cannot
for routine treatment take the place of guaiacol.
3.— The Naphthols.
Betol or Salicylate of /3-naphthol is a white,
lustrous, crystalline powder nearly inodorous, insoluble
in cold and hot water, soluble in boiling alcohol and in
warm linseed oil, decomposes in the intestines into
/3-naphthol and salicylic acid. Betol is less active than
/3-naphthol itself, and has therefore nothing to recom-
mend it. In all cases with intestinal disturbance.
P-naphthol is unrivalled, and its action is certain and
safe. Given in v — x-grain doses the intestinal canal, if
not rendered aseptic, is at least made less harmful, and
the further absorption of deleterious products prevented.
In about 5 per cent, of my hospital cases have I found
it called for, and the result has always been most
gratifying.
B.— Those substances which act by improving the general
tone of the organisms, and those whose action is more or
less indefinite.
Of this class the principal drugs are iron and arsenic.
It has not been stated even by the most ardent sup-
porters of these drugs that they play any specific rdle in
this disease. On the other hand, they have only been re-
commended as being those drugs which, from experience,
have been found most useful in so improving the gene-
ral health that the patient has been better able to with-
stand the inroads of the disease ; and, as such, they are
no doubt of great use. They are best administered
combined with one another, either in the form of a pill
or else in a mixture. The best preparation to use, of
iron, is either the tincture of the perchloride, or the syrup
of the iodide. Many prefer a preparation of iron and
quinine, or of the ammoniated citrate. Arsenic may be
1 38 RHEUMATOID ARTHRITIS.
given as the B.P. liquor, or as the liquor sodii arseniatis.
For the use of arsenic, we have the authority of Jenkin-
son, of Manchester, Beardsley, Charcot, Hilton Fagge,14
etc. M. Noel G-ueneau de Mussy recommended its use
externally in the form of arsenical baths. Iron alone, or
arsenic alone, is not nearly so successful as when the two
are combined.
Iodine, and the various iodides, are commonly held to
have a marked influence for good over the disease;
iodide of iron being specially lauded as an agent of
great value. Sir A. Garrod and Dr. A. E. Garrod 15 look
upon this drug as the most efficient we possess. It is,
however, probable that its usefulness depends mainly on
the iron, and not upon the iodide. Whether iodide of
potassium, or even pure iodine, has any direct effect on
the course of the disease it is difficult to prove or disprove,
but, personally, I have found little benefit from their use.
If they do act, they, probably, do so by virtue of their
alterative or eliminative powers rather than by any direct
action on the disease.
In a disease of such a nature it is no wonder we have
a large list of drugs, which have, at one time or another,
been recommended as sure and certain remedies. Of these
the following are a few : the alkalies, quinine, actsea raee-
mosa, fraxinus excelsior, colchicum, etc., which have been
and still are recommended ; but none of them are of any
lasting avail. Some have found benefit from the use of
the salicylates. Howard16 says that if sodii salicylate is
given in sufficient doses it promises well to be of use, in
the more acute forms, or in the actively inflammatory
periods and exacerbations, than any other form of agent.
Including See's cases Compagnon 17 has related seventeen
cases, in many of which the pain was relieved by its use,
and its progress arrested. Aetsea raeemosa according to
Einger is of use in full doses, especially if the uterine
TREATMENT. 139
functions are disturbed. Guaiacum has been recom-
mended by many, and has occasionally been found of use.
Lorenze and others mention iehthyol, but I have failed
to obtain equally good results. For the relief of
painful muscular cramps, Dr. Garrod uses hyoseyamus,
with good results.
C— Those substances which are of use when applied
externally.
These substances have been used almost entirely for
the relief of pain, and appear, except in the case of guaiacol
and carbolic acid applications, to have little other action.
Every known form of counter-irritant has been tried,
and of local applications there is practically no end.
Much of the good experienced from their use has been
the result of the friction, and massage associated with
their application. Chili paste ; turpentine ; paraffin oil ;
eamphor; ammonia; eajuput or eucalyptus oils ; liniments
of soap; ammonia, compound eamphor; iodine; eroton oil,
turpentine ; acetic turpentine or mustard ; have all been
tried. Of local remedies for the relief of pain, the
liniments of chloroform, belladonna, and aconite in equal
parts, applied on lint have often given ease. Dr. Spender
paints a ring of iodine one-and-a-half inches wide above and
below the joint. A eantharides blister may be tried on
the proximal side of the joint. Flannel dusted over with
flowers of sulphur is a popular remedy. Chaulmoogra oil,
cod-liver oil, oleate of mercury and morphine, unguentum
hydrarg*. eo., and others, have been used to rub into a
joint, or for strapping. All have their advocates, and all
are more or less inefficient. When articular pain is
severe, a local vapour bath or embedding the limb in hot
sand, as recommended by Trousseau, may give relief.
Guaiacum plasters in the more chronic stages have been
known to relieve pain. With regard to this pain all the
known hypnotics and analgesics have been at one time or
140 RHEUMATOID ARTHRITIS.
another employed with more or less success. Should the
local applications shortly to be mentioned not be success-
ful we have to fall back on the use of opium or morphia in
some of its forms, paraldehyde, ehloralose, sulphonal, etc.
Opium or morphia, as being the most certain, is pre-
ferable, and one often finds that after one or two good
nights the use of the hypnotic is no longer required.
The treatment I usually follow is, either to apply
guaiacol and equal parts of olive oil ; guaiacol in the pro-
portion of one to six of tincture of iodine, or else to use
warm carbolic acid fomentations. One not only gives great
local relief, but, by absorption, the drugs have a beneficial
effect on the disease itself. Guaiacol when applied ex-
ternally produces a numbness of the joint, a sense of
coolness and a feeling of relief. This effect becomes more
marked with every application, and the joint condition
often improves, simultaneously, in a most unexpected
fashion. But the great thing is the relief of pain. It
was first used as an application to painful rheumatic
joints by M. Desplats. He used equal parts of guaiacol and
glycerine, and painted it on, covering it with a dry dress-
ing. In three cases of arthritis deformans the results
were excellent. To mask the odour, oil of cloves is the best
according to Da Costa. Stolzeburg18 says this treatment
is accompanied by profuse sweats which it is unwise to
continue for any length of time. I have never noticed
these sweats. As a rule I apply it in equal parts with
olive oil, or else with tincture of iodine, in varying propor-
tions, that of one to six being my most common one
(iodine 6, guaiacol 1). It increases the flow of urine, and
reduces the body temperature. Applied externally ac-
cording to Drs. Linossier and Lanois 19 it is absorbed
rapidly, and can be easily detected in the urine. The
body temperature has been known to fall as much as 2°
after its application. Carbolic acid I use in the strength
TREATMENT. 141
of 1 in 40, and apply it warm as a fomentation. This
should be renewed every two or three hours. It acts
much in the same way as guaiacol, reducing the tem-
perature and acting as a local anaesthetic and analgesic.
It is rapidly absorbed, as can be traced in the urine. It
is not quite so efficient as guaiacol, but where the former
cannot be used, on account of its odour, it is of use. It
may also be tried with advantage where guaiacol is not
very successful, as occasionally happens in the acutely
neurotic patients.
III. — Electrical, Thermal and other special
Modes of Treatment.
1. Electrical Treatment.— The weak continuous current
(15 to 25 Leclanche cells), used twice a day, may be of
service. The sponge electrodes being well moistened in
hot salt and water, one is placed above the affected joint,
and the other over the skin at any part of the limb
distal to the joint to be operated upon. Even the induced
or interrupted current may be employed. I never use
either during the acute stages, but later on when the
disease has been subdued, and only weakness, and
atrophy remain, I have found great benefit, especially
from the weak continuous current. Erb 20 treated a large
number of cases by galvanism, and although having no
absolute cures he has met with occasional good results,
as far as improvement of the general state of nutrition,
and of the local troubles were concerned. He considers
it better to apply it direct to the spine than to the sympa-
thetics. When the upper extremities are mainly affected,
he passes the current through the cervical cord, and
when the lower extremities are the principal offenders,
the lumbar cord. It is recommended to continue the
treatment for several months, but few patients will
persevere with so prolonged a course. Dr. Steevenson
142 RHEUM A TOW ' ARTHRITIS.
and Dr. Garrod both mention the use of the electric bath.
They consider that it exercises a favourable influence
over the course of the disease. A bath tub is used of
some non-conducting material, such as wood or porcelain,
and this is filled with water at about the normal tem-
perature of the body. A copper plate connected with the
negative pole is placed at the foot of the bath, and a
similar plate at the head is in connection with the posi-
tive pole. A galvanometer, measuring at least 250
milliamperes is used. The strength employed is about
^00 milliamperes, and it is computed that only 40 pass
through the body, while the remainder pass through
the water. The full current of 200 milliamperes is
used for about ten minutes. During the first six days
the bath is given daily, and afterwards every second
day.
2. Thermal Treatment. — Treatment by means of hot
mineral waters, and other accessories is of the greatest
value. To the consultant the choice of a suitable thermal
water becomes of the first importance, but unfortunately
no fixed rules can be laid down. In some cases the
alkaline, or indifferent, and in others the sulphurous
waters appear to answer best. Of the alkaline, or indif-
ferent, Bath and Buxton in this country are the most
frequented. Owing to its situation Bath is much warmer
than Buxton in winter, and in the majority of cases is
more suitable. In summer Buxton is preferred by
many. Of the sulphurous, Strathpeffer has latterly
come to enjoy considerable repute as a summer resort,
whilst Harrogate still maintains its ancient character for
efficiency. Amongst the many other spas in this country
are Woodhall (Iodine), in Lincolnshire, and Llangammareh
(Bromine), in Wales, both of excellent service in certain
cases ; but for the average case the indifferent or alkaline
waters are preferable. And of these, Bath maintains
TREATMENT. 143
its premier position. Abroad we have the thermal waters
of Wildbad, Carlsbad, Wiesbaden, Toplitz, Homburg", Kissin-
gen, St. Moritz, Bourboule, Mont D'Or, Aix-les-Bains,
Hammam R'Hira and Hammam Meskoutin, and Arkansas,
Virginia, and Banff, in America. When anaemia and de-
bility are prominent symptoms, the chalybeate waters of
Langen Sehwalbaeh, Rippolsau, Spa, Franzenbad, etc., are
of use. At Aachen special attention is paid to rheumatoid
arthritis by means of douches and massage in conjunc-
tion with the general baths. Eademacker 21 has found
great benefit from this plan of treatment, even in ad-
vanced cases.
The Bath thermal waters have been used for ages in
this as well as in other joint complaints, and have come
to possess a name and repute, for alleviating the symp-
toms of such disorders, second to none — in fact so much
so that due discretion is not always observed either by
the bathers or their medical advisers. Beyond all doubt
they are most useful in the early stages, and again, when
the disease is subdued, they come to be almost equally
invaluable. But no greater mistake can be made than
to imagine that they will cure all and every condition.
I hold that alone, during certain stages, they, like all other
mineral waters, are not of the smallest use, but given
a proper, and successful medication we derive much help
and good from them not only in alleviating symptoms,
but in counter- acting the effects of stiffness, deformity,
and muscular weakness. I know of no waters, in this
disease, of more avail than those of Bath. It has been
said more than once that patients have derived no bene-
fit from our waters, but so it may be said of any waters.
Combined with suitable internal treatment, which must
often be of a prolonged nature, no case should leave Bath
unrelieved if not cured. But we must make it clear that
once a joint is disorganised no power on earth can renew
144 RHEUMATOID ARTHRITIS.
the diseased tissues. We may alleviate and relieve pain,
give greater movement, and, in short, make life bearable,
but we cannot make a joint quite perfect — there must
always remain some symptoms to show how severe the
attack has been. In severe and advanced cases improve-
ment can only be obtained after months of treatment, a
period often most trying both to the patient and the
physician in charge.
At first, immersion in the waters acts as a gentle
counter-irritant — the gentle excitation of the cuticle
being passed by reflex action throughout the body —
an increased oxidation and production of heat being the
result. The circulation improves, and the tissues receive
fresh supplies of blood to reinforce their vital powers.
Again wet and dry douching stimulates and exhilarates.
The latter has to be used with care, as where the joints
are sensitive it may do much harm. If practised as at
Aix-les-Bains much benefit may be derived from it, how-
ever. In Bath this system has been carried to high per-
fection, where the attendants are not only highly qualified,
but do their work with a thoroughness and care not often
met with. The massage or shampooing combined with
the douching has often a marvellous effect in the chronic
stages. By its means the muscles are strengthened
and further atrophy prevented, and it also seems to have
a soothing effect on the joint pains and nerves. It is also
of use in the insomnia which so often accompanies rheu-
matoid arthritis. When practised dry it appears to have
a more exciting effect, and its results are not altogether
so good. Massage again, where walking is difficult or
impossible, keeps the muscles healthy and the skin in a
condition of activity. It may be employed along with
electricity, but certainly its best results are obtained
when it is carried out in a bath by a skilful operator. When
the attack is acute, only the lightest and slightest
TREATMENT. 145
massage is permissible. As the joints stiffen it
may become more forcible, and deeper, and should
be combined with passive movements, under which
treatment deformities and ankylosis often improve
and do well.
In Bath we have one of the finest bathing establish-
ments in existence, filled with all the necessaries and ac-
cessories so essential to the comfort of the invalid. Bathing
may be carried out with or without the douche ; douching
with or without wet or dry massage ; local vapour baths ;
specially prepared mud ; medicated and electric baths; and
baths and douches for special organs. The waters them-
selves are drunk not only on account of their constituents,
but from the fact that they help to wash out impurities
of the blood by flushing the kidneys ; thus assisting the
elimination of toxic products. The baths also act in a
two-fold fashion, assisting the elimination of the toxic
materials through the skin and lungs, as well as assisting
in the improvement of the more purely mechanical
defects.
Care must be taken not to push thermal treatment to
such an extent as to debilitate the patient, and, therefore,
it is probable that the course should cover a long period,
with baths at considerable intervals, rather than a large
number crowded into a short time.
Should it not be possible for a patient, as alas ! too
many cannot, to go to a spa for treatment, by careful
bathing in a slightly alkaline warm bath, much may be
done at home. Massage and rubbing can usually be
obtained anywhere, and gymnastics can be improvised.
What answers well is a gentle course of gymnastics,
pulleys, dumbells or elastic bands with handles, all of
which if not carried too far are of much use.
Within the last year or so, the hot-air bath has been
used and found to be of much benefit, but only in the
10
146 RHEUMATOID ARTHRITIS.
more chronic cases, and where the disease is not
extensive.
I must now for a moment glance at certain other
methods and systems of treatment for special conditions.
If pain, as we so often have in the knees, is severe, and
apparently from the rubbing of the ulcerated cartilages
one upon another the only method to deal with this is by
extension by weights. Where fluid is exuded we seldom
come across this difficulty, but now and again we see it,
and are often puzzled as to the best means of subduing
it. The weights should not be hea^y, bat should be
applied continuously. Again, should there be an excess
of fluid present it may be desirable to tap the joint, and
withdraw the fluid. I have often seen the mere fact of
puncture relieve tension and give ease. One should not
therefore be discouraged if no fluid is found. I find
patients once relieved by this means ask for it to be done
again and again. Should the jaws become either totally
or partially ankylosed. we are on the horns of a dilemma.
If only partially ankylosed, probably a series of small
blisters will relieve the difficulty (I never apply one
larger than a shilling piece). Should it be unrelieved, we
have to consider the advisability of excision. This has
been done in several cases with fair success. It has
also been practised on other joints, such as the knee or
elbow, where there was little power and great crippling.
In three cases I have seen the result, which was fairly
successful in two. In both there was before operation
great deformity, and the limb was useless, not so much
from pain as from inability to use it. In both, bony
ankylosis ultimately resulted and there was no return of
the disease in those joints. Of course the other joints
remained in statu quo ante. In the other case, the pain
and disease returned within a few months, probably from
an insufficiently extensive operation. In a few cases I
TREATMENT. 147
have recommended the operation as desirable, but in all
it was declined. My personal knowledge therefore on
this subject is slight.
Climate.— Whatever may be said, there can be no
doubt, that those who can afford it should not winter in
this country. Egypt is par excellence the place for such
to winter. Biskra and some of the other Algerian health
resorts are nearly as good. What one has to bear in
mind is that it is a dry warm atmosphere which is
required, not a dry or a damp cold one. The northern
Mediterranean sea-board, except during mild winters,
and except in a few spots is not advisable. It is better
to live at home where all the comforts and necessities
are so much better and more easily obtained. For those
who have the time, and money, a winter in the dry
Karoo of South Africa is of advantage. I am not in
favour of a long sea voyage, nor yet of residing near the
sea. The moisture is invariably undesirable. A voyage
often, by mere rest and absence of anxiety, may do
wonders, but as routine treatment it is not advisable.
To Summarise. — In the acute stages, the patient should
be kept in bed, on a light nutritive diet. The joints may
be kept at rest, by a light splint, and painted with guaia-
col and olive oil or iodine, or else fomented with carbolic
acid solutions. Internally guaiacol carbonate or benzosol
should be given. If sleep is not readily obtained, this
must be attended to, as must also be the gastrointestinal
and genito- urinary tracts. If the patient can stand it,
light massage, and baths for short periods, as may be
ordered. As it becomes more chronic the patient is
allowed up, and the thermal treatment pushed — electricity
and gymnastics often now being useful. The diet must
be carefully supervised, and the use of cod-liver oil and
maltine being now indicated. Internally, the treatment
as in the acuter stages.
148 RHEUMATOID ARTHRITIS.
THE BATH THERMAL WATERS.
The springs which supply the waters of Bath are three in num-
ber, giving a daily yield of 507,600 gallons, at a temperature of
117°-120° Fahr. If compared with other thermal waters of
Europe and America, we see that those of Bath stand high in the
scale.
EUROPE :
Germany,
Fahr.
Aix-le-Ckapelle (Kaiserquelle) 131-0°
Baden Baden (Hauptqulle) 155*4°
Ems (Kesselbrunnen) 11 8*4°
Karlsbad (Mlilbrunnen) 1360°
Karlsbad (Sprudel) 164-0°
Karlsbad (Schlorsbrumien) 134'4°
Neuenahr (Mariensprudel) 101'7°
Schlangenbad 82*4°
Warmbrunn 104*0°
Wiesbaden 1 5-6°
Willbad 94.0°
France,
Aix-les-Bains 110*3°
Luchon 131-3°
Dax 140-0°
Mont Dore 105-8°
Bareges 111'0°
Italy,
Baltaglia 160-0°
AlJSTRO-HUNGARY,
Baden 96'8°
Toplitz (Hauptquelle) 120*0°
Gastein 87*0°
Switzerland,
Leuk 123-0°
England,
Bath : 120-0°
Buxton 82-0°
AMERICA :
Hot Springs, Garland, Arkansas 93-0°-150-0°
Chalk Creek Hot Springs, Colorado 130-0°
Des Chutes „ ,. Oregon 143°-145-0°
Madison Co. „ „ N.Carolina 102-0°
TREATMENT.
149
If compared with the waters of Buxton, those of Bath are seen
to be much stronger : —
In an Imperial Gallon.
Bath.
Buxton.
Carbonate of Lime
9-001
0-399
1-217
15-017
69-984
6-702
35-042
23140
17-894
1-823
0-399
1-562
9-185
,, Magnesia
,, Iron
,, Soda
Sulphate of Ammonium
,, Lime
4-746
0-037
0-014
0-673
,, Potash
„ Magnesia
,, Soda
Chloride of Sodium
0-678
0-202
4-517
,, Potassium
Silicate of Soda
Nitrite of Lime
0-266
In an Imperial Pint of the Bath Waters there is: — Oxygen 0-74 ;
Nitrogen 4*60 ; Carbonic Acid 417 cubic inches.
The total solids in each pint of the Bath waters is 168 grains.
The amount of the gases, free and in combination, is of the utmost
importance, as they act as powerful stimulants by the excitation
of the cuticle which they produce.
Compared with other waters we find the total amount of solids
in each gallon to be : —
Kissingen 884-000
Marienbad 649-750
Baden 340-000
Karlsbad 496-071
Bath 168-400
Mont Dore 114'360
Toplitz 48740
Warmbrunnen 40-380
Willbad 35-870
Gastein 26*680
Romerbad 22-370
Buxton 20-579
Plombieres 20-170
REFERENCES.
1. Hudeod. — " Creasote et Tuberculose," Geneve, 1893.
2. Powell, Douglas. — " Diseases of the Lungs," p. 549.
3. Hoelscher.— " Berlin Klin. Woch.," 1892, No. 3.
4. Bates.—" New York Med. Journal," 1893, April 2.
150 RHEUMATOID ARTHRITIS.
5. Bouchard and Gimbert. — " Gaz. Hebdomadaire," No. 31,
1877, p. 488.
6. Jaccoud.— " Gaz. Hebdomadaire," No. 31, 1877, p. 156.
7. Rosenthal.—" Berlin Klin. Woch.," No. 32, 1888.
8. D'Or.— " Rev. cle Medicin," February, 1890.
9. Rosenbach.— Cited. " Med. News," April 28, 1888.
10. Flint.—" New York Med. Journal," July, 1890.
11. Bogdanovitch.— Cited. " Brit. Med. Journal," vol. i., 1888.
12 Sahli.— " Correspb. f. Schweitzer Aertze," 1887, No. 30.
13. Picot.— " Semaine Medicale," 1891, March 14.
14. Fagge, H. — " Principles and Practice of Medicine."
15. Garrod. — " Rheumatism and Rheumatoid Arthritis."
16. Howard. — " Pepper's System of Medicine."
17. Compagnon. — " De l'utilite du Sal. de Soude dans le Treat-
ment du Rheum atisme," 1880.
18. Stolzeburg.— " Berlin Klin. Woch." No. 5, 1894.
19. Linossier and Lanois.— " Union Medicale," April 1894.
19a. Anders, J. M.— " Therap. Gazette," March 15, 1895.
19b. Champonniere. — "Bull, de TAcadamie de Medicine," July 30,
1895.
20. Erb.— " Handbuch der Electropathie," s. 648.
21. Rademacker. — "Aachen als Kurart," s. 111.
i5i
CHAPTEK VII.
SENILE ARTHRITIS.
Morbus Coxae Senilis — Senile Arthritis —Monarticular Rheuma-
toid Arthritis — In whom seen — Symptoms — Morbid Anatomy
— Changes in the Bones — Trophic Phenomena — Treatment.
Morbus eoxse ssnilis, senile arthritis, or as many call
it, monarticular rheumatoid arthritis, is most typically
seen in the hip-joints of elderly people. It has been
maintained, by some, that it is a similar condition to
rheumatoid arthritis ; but to this I cannot agree. For
one thing it does not involve the peripheral joints, being
confined almost entirely to the hips and shoulders. It
is unaccompanied by any nerve or trophic phenomena,
and the muscular wasting present is merely that induced
by disuse, and mal-position of the bones. Taking it all
round, it is quite distinct both clinically and patho-
logically. It is usually monarticular, but not invariably
so, and, as I have said, principally affects the hips or
shoulders. There is no symmetry, and it is most
common in men — women more rarely being affected.
It, as a rule, follows some injury of a very trifling
nature. With diseased arteries and tissues whose vitality
is impaired it is possible, nay probable, that an injury
may so affect the joint structures, both through their
vascular and trophic supply, that a joint lesion may
follow on what would otherwise be the most harmless
incident.
Adams first gave it the name of " Malum coxa3
Senile," but later on substituted " Chronic Eheumatic
152 RHEUMATOID ARTHRITIS.
Arthritis." Much has been written on the subject,
and amongst others, we find Kobert Smith,1 Colles2 and
Wilmot3 have done so with special reference to the
disease as it occurs in the hip joints. Canton4 refers to
a similar condition in the shoulders, and Geist5 describes
the disease as a form of senile gout.
Symptoms — As a rule, the disease begins as a gnaw-
ing pain, which speedily results in the loss of the use of
the limb. If in the hip, the pain is often referred to
the knee likewise, but, as a rule, the principal pain is
felt over the trochanter or else in front in the groin. The
pain is rarely, at first, so severe that the limb cannot be
used, but, in the later stages, it may become marked. It
is found the patient cannot cross the affected leg over
the unaffected one, without using his hands. There is
inability to rotate the limb, and there is atrophy of the
gluteal muscles, as well as of the muscles of the thigh.
The tendon reflexes are increased. As the disease pro-
gresses we have considerable shortening, owing to
absorption of the head of the bone. There may be
eversion with some adduction. The movement of the
joint is limited and attended with considerable pain,
and distinct grating. The symptoms in the shoulder,
are somewhat similar. The arm cannot be raised from
the side, and any attempt to do so causes acute pain.
When at rest the pain is not so acute as in the case of
the hip. Again, in the case of the hip we may, occa-
sionally, find cysts sometimes intimately in connection
with the joint; but in others, at some distance from and
free from it. They vary in size and are filled with
thick, glutinous, straw-coloured fluid. As the progres-
sive shortening of the limb proceeds, we have thickening
of the trochanter, from the deposition of lime salts
about its base, and it seems unduly prominent from
the muscular wasting. The pelvis is often raised on the
SENILE ARTHRITIS.
153
diseased side, as the patient, by introducing another
joint, by walking on the toes, hopes to prevent shocks
and jars to the diseased parts. The toes may be turned
in or out, but more usually the latter.
Post Mortem. — We find the joint distorted, the liga-
ments thickened, and the synovial membrane the seat
of chronic inflammatory changes. The articulating sur-
faces are worn down — the cartilages being altogether
destroyed or else still remain in patches, showing the
bone here and there bare underneath. What remains of
the cartilage can be easily stripped off, showing a rarefied
condition of the bone. Instead of being hard and indur-
ated, as one would find in the chronic stages of rheuma-
toid arthritis, we find it soft
and yellowish in appearance,
and it breaks down readily —
apparently due to general wast-
ing of the bone with fatty de-
generation of the medullary
substance. In the case of the
hip, the neck may become so
absorbed, that the head comes
to rest on the trochanter.
There may be an apparent
widening of the acetabulum
from the same reason. Occa-
sionally there is true new bony
formation around the neck, but
this is rare.
round the articulating surfaces. The disease consists
in a pure degeneration or wasting of the bone, followed
by that of the cartilage. The changes in the bone are
the primary and principal ones, those in the cartilages
and synovial membrane being secondary. The bone is
characterised by an increase in the number of its
Fig. 9. — Head, of femur from a
case of Morbus Coxae Senilis. A,
ulceration, exposing softened bone,
and B, neck greatly absorbed, with
It maV also OCCUr sli§'nt deposition of lime salts.
154 RHEUMATOID ARTHRITIS.
spaces ; the trabecular are fewer in number ; thinner
and farther apart, and the spaces are filled with a
yellowish marrow, consisting of round cells, granular
corpuscles, and others having undergone fatty degenera-
tion. It differs widely from the bone marrow in normal
bone, and also from that found in true rheumatoid
arthritis.
The disease appears, to me, to be a pure degeneration,
due to some trophic or vascular malnutrition. With
regard to treatment, nothing can be done beyond pallia-
tion. Eelief of pain is our principal object, and is
accomplished, more or less inefficiently, by the use of
local applications, such as belladonna, small blisters, the
continuous current, massage, bathing, etc. By good
feeding, rest and stimulants, the progress of the disease
for a time may be arrested, leaving only a permanent
disorganisation, which nothing can repair.
REFERENCES.
1. Smith, Robert. — " Dublin Jourii. of Med. Sciences," 1835, vi.
kl. Colles. — Quoted Garrod, "Rheumatism and Rheumatoid
Arthritis."
8. Wilmot.— Quoted Garrod, loc. cit.
4. Canton.—" London Med. Gazette," 1848, N.S., vi.
5. Geist. — " Klin, der Greisenkrankheiten Erlanger," 1860.
APPENDIX.
i56
APPENDIX.— Table of Cases
Family History.
Previous History.
Joints
1
1
F.
31
Negative
Began in neck
2
F.
37
■)•> • • • • • •
2
2
3
M.
44
,, ... ...
In wrist after getting wet
2
2
4
F.
31
,,
In fingers
2
2
5
F.
35
,,
In fingers
2
6
F.
33
,,
In hands after acute rheu-
matism
2
2
7
F.
55
,,
In fingers
2
2
8
F.
53
,, ... ...
In right knee
2
2
9
M.
50
,,
In ankles
2
2
10
F.
29
j? • • • • ■ ■
In wrists
2
11
F.
30
jj • • • ■ • •
In fingers
2
*2
12
F.
23
}9 • • • • • •
In fingers
2
1
13
F.
33
5/ • • •
In hands after concussion
of spine
2
2
14
F.
47
In wrists from hard work...
2
2
15
F.
34
Mother had rheumatic
gout ...
In ankles
2
16
F.
39
Negative
In knees after confinement
1
1
17
F.
52
>j • - • • • •
In wrists
2
2
18
M.
63
,, ... . . .
In hips
1
2
19
F.
27
,, ... . . .
In hands after acute rheu-
matism
2
2
20
F.
36
;; ... . . .
In hands after confinement
2
2
21
F.
55
Father had rheumatoid
Began after acute rheuma-
arthritis
tism
2
2
22
F.
44
Negative
In hands during pregnancy;
got worse after confinement
2
1
23
F.
23
Rheumatoid arthritis
In hands after acute rheu-
in mother ...
matism
2
1
24
F.
31
Negative
After chronic rheumatism
2
2
25
F.
39
,,
2
2
26
F.
25
,,
After acute rheumatism . . .
2
1
157
and Analysis of Symptoms.
o
1
t-2
W
'3
<
CO
1
2
2
2
2
1
1
2
1
1
1
2
2
1
2&
toes.
1
1
1
1
1
2
2
1
1
2
1
1
I
1
1
2
1
1
2
1
1
1
2
2
1
1
2
2
■*1
1
2
1
1
1
1
2
2
1
2
1
1
2
2
1
1
2
1
1
2
2
1
1
1
1
1
2
1
1
1
2
2
Other Symptoms.
Patient very hysterical..
Dyspeptic...
Sweating palms, emacia-
tion, dyspepsia
Sweating palms, recent
pigmentation ...
Cardiac
Had recent subconjuncti-
val injection of both eyes
Sweating, emaciation,
pigmentation ...
Sweating, cardiac
Sweating, pigmentation,
dyspepsia
sacrum.
Cardiac
Emaciation
Sweating, pigmentation,
dyspepsia
Emaciation
Sweating, pigmentation,
emaciation
Sweating, pigmentation,
emaciation
Dyspepsia
Dyspepsia
Sweating, pigmentation
Result.
Very much better.
Unchanged.
Better.
Better.
Unchanged.
Unchanged.
Better.
Very much better.
Much better.
Much better.
Very much better.
Very much better.
Unchanged.
Much better.
Better.
Better.
Better.
Much better.
Much better.
Better.
Unchanged.
Much better.
Much better.
Much better.
Better.
Unchanged.
1 58
APPENDIX
F.
47
F.
22
F.
39
F.
84
F.
43
F.
45
29
F. ! 24
51
M. ■ 56
F. ' 34
F. 33
F. 60
F. I 11
F. I 30
F. J 29
F. 41
M.
F.
F.
F.
59
49
32
30
Family History.
Negative
Son suffered from hae-
morrhagic rheuma-
tism ...
Rheumatoid in father ;
sister had chorea . .
Negative
Rheumatoid history on
mother's side
Negative
F.
42
F.
48
F.
19
F.
50
F.
24
F.
30
Previous History.
In left elbow...
After acute rheumatism . .
In fingers after necrosis of
jaw from decayed teeth
In hands
In fingers with haemorrhage
under nails
After confinement ...
In feet after acute rheuma
tism
In hands after acute rheu-
matism
In ankles
In fingers
After confinement ; previous
history of acute rheuma
tism
In feet
In wrists
In hands
In hands after a chill
In hands after acute rheu
matism
In knee after miscarriage .
In fingers after hard work
In hands after acute rheu-
matism
In right hand after chronic
rheumatism
In shoulders ...
In hands after two attacks
of acute rheumatism
In knees after getting wet
In knuckles ...
In hands after hard work
H
•4J
£ »
%
M.g
o
^ H
.a
a*
H
W
2
2
2
2
2
2
2
1
2 | 2
2 2
2 1
[Continued).
159
1 1
1 I 2
1 I 2
1 I 2
Other Symptoms.
Result.
Better.
...] Very nmch better.
Sweating, emaciation ... Better.
... " ! Better.
Much better.
Cardiac
Sweating, pigmentation,
emaciation
Sweating,
cardiac
emaciation,
Emaciation, cardiac
Pigmentation
Sweating-
Cardiac
Sweating, pigmentation
Sweating, pigmentation
Sweating ...
Much better,
Very much better.
Better.
Unchanged.
Unchanged.
Better.
Better.
Unchanged.
Unchanged.
Very much better.
Much better.
Better.
Better.
Unchanged.
Emaciation, cardiac ... Very much better,
Sweating ...
Emaciation
Sweating ...
Sweating ...
Sweating, pigmentation,
emaciation, cardiac ..
. Better.
. Better.
Much better.
Better.
Better.
Much better.
Better.
i6o
APPENDIX
w j
F. 19
M. j 33
56 F. I 28
57 F. ; 32
F. ! 50
59 I F. 48
60 M. : 48
61 F. 50
62 i F. 42
63 F. 52
64
M.
42
65
F.
21
66
F.
38
67
F.
30
68
F.
28
69
F.
45
70
F.
36
71
F.
39
72
F-
28
73
F.
15
74
F.
28
75
M.
48
76
F.
34
77
F.
37
78
F.
59
Family History.
Negative
Previous History.
In hands after getting wet
In hands after acute rheu-
matism
In left shoulder
In fingers
After acute rheumatism . .
In feet after diphtheria ..
After acute rheumatism . .
In wrists
In wrists after acute rheu-
matism
In ringers
In left foot
After influenza
In fingers
After acute rheumatism .
After acute rheumatism .
Joints
,3
2
2
2
2
2
2
2
1
2
2
In hands after acute rheu-
matism
In hands after confinement
In knee after fractured
patella
After acute rheumatism ... 2
In feet and hands after
acute rheumatism ... 2
In right hand after tonsillitis' 2
i In ankles j 2
! 2
The folloiving is a short synopsis of the more rare coincident complications
17 had pigmentation; 14 were emaciating rapidly ; 1 had cedema of the feet; 1
(Co?iti?iued).
161
Affected.
A4
xh
o
£
ft
1-3
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
l
1
1
1
1
1
1
1
1
1
1
1
1
1
sac
rum
"i
1
i
1
i
1
i
1
2
1
*2
l
2 i
- i
2 i
Other Symptoms.
Result.
Pigmentation
Cardiac
Sweating, pigmentation
emaciation, cardiac
Cardiac
Sweating, pigmentation
oedema of feet...
Sweating ...
Sweating ...
Pigmentation
Cardiac
Sweating, pigmentation
Sweating, flushings, pig
mentation
Cardiac
Cardiac
Sweating, pigmentation
emaciation
Emaciation
Sweating, emaciation
cardiac
2
Much better.
Much better.
Much better.
Better.
Better.
Much better.
Better.
Better.
Better.
Better.
Better.
! Better.
Unchanged.
Better.
Much better.
Much better.
Better.
Much better.
Much better.
Very much better.
Very much better.
Very much better.
Better.
Unchanged.
Better.
observed in the above cases : — 14 suffered from heart disease ; 25 had sic eating palms
had flushings ; 1 subconjunctival hcemorrhages ; 1 hamorrhages under nails.
11
l62
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Ball. — " Du Rheumatisme Visceral," These de Paris, 1866.
Bates. — ■" New York Med. Journal," 1893, April 2.
Beau.—" Gazette des Hopitaux," 1864, July 19.
Beauvais, Landre. — " Goutte Asthenique Primitif," 1800.
Besnier. — " Diet. Encylclop. des Sciences Med.," 1876.
Bezancon. — " Annales de l'lnstitut Pasteur," February, 1895, and
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Billroth. — " Gen. Surgical Pathology and Therapentics," (transl.)
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Bristowe. — " I>rain," 1888, vol. x.
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Brodie. --" Diseases of the Joints," 1833.
Campagnon. — " De Putilite du Sal. de Soude dans le trait, du
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Canton. — "London Med. Gazette," 1848, N. S., vi.
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Cruveilhier. — " Anat. Pathologique," Liv. ix.
Darkschewitsch. — " Neur. Cent.," 1891.
Davies, Lloyd. — " Lancet," vol. ii., 1893.
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De Sauvages. — " Nosolgia Methodica,," class vii., order i.
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Dori, Lacaze. — " These de Paris," 1832.
BIBLIOGRAPH Y. 1 63
Drackmann.— " Nordiskt. Med. Arch.," 1873, v.
Duckworth, Sir D.— " Heath's Diet, of Pract. Surgery," 1886,
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Duckworth, Sir D.— " Treatise on Gout," 1889, and "Brit. Med.
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Evans. — " Brit. Med. Journal," 1891, vol. i.
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Ewing. — " Lancet," vol. i., 1894.
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Flint.—" New York Med. Journal," 1890, July.
Foder.— " Centralb. f. Bakt. u. Parasitenk.," February 28, 1895.
Folli. — "II Policlinico," December, 1894.
Forsbrooke. — " Dissert, on Osteo-arthritis," 1893.
Fuller. — " Rheumatism, Rheumatic Gout and Sciatica," 1852.
Garrod, Dr. A. E. — "Rheumatism and Rheumatoid Arthritis,"
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Garrod, Sir A. — " Gout and Rheumatic Gout," 1876.
Geist. — " Klin, der Greisenkrankheiten Erlangen," 1860.
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Gowers. — " Diseases of the Nervous System," vol. i.
Griffiths. — (see Lane.)
Gwilt. — " Handbuch der Path. Anat."
Habershon.— " Brit. Med. Journal," 1892, vol. i.
Hadden.— " Trans. Med. Soc," New York, 1886.
Haller. — " Elementa Physiologica," vi.
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Hoffa.-" Volkmann. Klin. Vortrage," 1892.
Homolle.- " Diet, de Med. et Chir. Prat." 1882.
Hoppe-Seyler. — " Virchow's Arch." 1872.
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Hutchinson. — "Pedigree of Disease," 1884, and "Med. Times
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Jaccoud. — " Gaz. Hebdomadaire," No. 31, 1887, and " Lecon de
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1 64 RHEUMATOID ARTHRITIS.
Key.— " Med. Chir. Transact.," 1833, xviii.
Kohts.— " Berlin Klin. Woclienschr.," 1873.
Kolliker. — -" Elements of Human Histology,"
Kussmaul. — "Arch, fiir Pbysiolog. Heilkunde," vol. xi., 1852.
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Laken— " Centralb. f. d. Med. Woch.," 1887.
Lane, A. — " Path. Soc. Transactions," 1884 and 1886.
Lane, H., and Griffiths. — " The Rheumatic Diseases " (so-called),
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1 66
INDEX.
PAGE
PAGE
Aachen
143
Arsenic
137
Aconite
139
Arthrite Seche
6
Actsea raceinosa
138
Arthritic Diathesis
16
Acute Rheumatism, diagnosis
Arthritis, Chronic Rheumatic
3
of
93
— deformans
4,8
Acute Rheumatoid Arthritis
87
Arthropathies, nerve
92
age at which it
Aspiration of joints
146
occurs
87
Ataxic paraplegia
28
appearance of joints
Atmospheric conditions, a
in
89
cause
21
cardiac troubles in
90
Atony of muscles
111
fever in
90
Atrophy of the skin, etc.
121
in children . .
88
muscular atrophy in
90
Bacillus, cause of the
pain in
90
disease . . . . 12, 71
pigmentation in . .
90
— mode of growth . .
76
Adams 3, 6, 9, 16, 18, 48, 4£
), 56
— shape of
74
Adhesions
55
— staining of . .
73
iEtiology
12
— pyocaneus . .
40
Age, as a cause
18
— tuberculosis
40
Aix-la-Chappelle
148
Bacteria, pathogenic
13
Aix-les-Bains . .
148
effect on joint tissues
34
Albumoses
45
effect on endocardium
Alcohol
31
and pericardium . .
14
Alcoholic Muscular Atrophy
115
where they propagate
14
Alkalies
138
Bacterial products . . 15, 35
Alkalinity of the blood
23
how absorbed . .
35
Alimentary tract, symptoms
selective action of
36
due to
123
their action on nervous
Ammonia
139
system
36
Anaemia . . . . 26, 41,
118
Baden Baden
14S
Anatomy, morbid
48
Baker, Mr. Morant
101
Adams' views on
6
Ball
112
Anders
135
Ballet
116
Ankylosis
104
Banff
143
— bony
61
Bareges
148
Adams on
6
Barlow
88
Cruveilhier on
6
Bath
142
— fibrous . . . . 51,
104
— waters
148
Anterior cornua, multipolar
constituents of
149
nerve cells of
37
effect of
144
Anthrax
14
how used
144
Arkansas, hot springs
143
suitable cases for
143
Arloing
.
40
Battaglia
148
INDEX.
[6;
PAGE
Beardsley 138
Beau Ill, 112
Beauvais, Landre . . . . 5
Belladonna 139
Benzo-naphthol . . . . 123
Benzosol . . . . . . 132
— nature of and mode of
administration . . . . 136
Besnier 7, 56, 112
Betol 137
/SNaphthol 137
Bezaneon . . . . 36
— on toxic action . . . . 40
Billroth 49
Blaxall, Dr., report on micro-
organisms . . . . 72
Blisters 139
Blood, action of toluylene-
diamin on . . . . . . 43
— changes in . . . . . . 66
— destruction of . . . . 42
— in joints . . . . 57
Bocker 123
Bone, appearances of 51, 60
— erosion of . . . . . . 62
— hypertrophy of . . . . 61
— rheumatoid changes in . . 4
Bone marrow . . . . 62
Bones, enlargements of . . 100
— nodules of . . . . . . 100
Bonnet.. .. .. .. 114
Bony-loose-bodies . . 54
Bouchard, on toxic action . . 40
Bourboule waters . . . . 143
Bowlby 61
Bristowe, Dr 118
Broca 3, 6
Brodie 6
Bronchitis 123
Brown-Sequard . . . . 33
Bulbar warnings, Dr. Spender
on 31
Bursse 100
Buxton 142
Cajuput 139
Calcium phosphate in urine 123
Campagnon . . . . . . 138
Camphor . . . . . . 139
Canton 6,152
— on Senile Arthritis in
Shoulder 152
Carbolic Acid, external appli-
cations of . . . . .. 140
PAGE
Cardiac condition, due to
micro-organisms . . . . 112
Cardiac lesions, statistics of 113
Carsbad
Cartilage, appearances of . . 51
— Billroth on 57
— changes in . . . . . . 57
— Cornil and Ranvier on . . 58
— fibrilation of . . ..58
— marginal overgrowths of 60
— osseous changes in . . 60
— prolification of . . 58, 59
— Rindfleisch on . . 57, 59
Cartilaginous changes 7, 57
— loose bodies . . . . 54
Catarrh of mucous mem-
branes
Causes
Cause, age as a
— atmospheric conditions as a 21
— catarrh of mucous mem-
branes as a . . . . . . 19
— emotional causes as 21
— genito-urinary complaints
as a . . . . . . . . 19
— heredity as a . . . . 15
— injury as a . . 22
— sex as a . . . . . . 17
Cavafy 67
Cazin 29, 37
Central nerve system, degener-
ation of . . . . 63
Champonniere . . . . 3 35
Changes in the joints . . 50
Charcot 1, 3, 7, 16, 21, 25, 66, 69,
84, 86
classifica-
12, 19
.. 15
. . 18
of
— his method
tion . .
— on deformities
— on heredity
— on skin changes
— on tachycardia
Charcot's thesis
— views as to the pathology
— joint disease
Charrin
Chaulmoogra Oil
Chiaje
Children, rheumatoid arth
ritis in
Chili Paste
Chloralose
Chloroform
Cholesterin
Chomel
84
107
16
122
117
7
25
92
40
139
4
90
139
140
139
56
5
1 68
INDEX.
PAGE
PAGE
Chromatogenic functions of
Deville
. 3,6
the skin
122
Diagnosis
. 92
Chlorosis
41
Digitorum nodi
. 3
Chronic Rheumatic Arthritis
3
Diphtheritic muscula
r
Chronic Rheumatism of the
atrophy
. 115
joints
3
Dislocations
. Ill
Chronic Rheumatoid Arth-
Dori, Lacaze
. 7
ritis 84, 91
Douche baths. .
. 144
— its characteristics
91
Duckworth, Sir Dyce 8, 17,
18,26
Choostek
49
on deformities
. 107
Circulatory system, symptoms
on Heberden's nodes
. 70
due to
116
Duplay..
. 29
Climacteric
18
Dyspepsia
. 123
Climate
147
Dystrophic theory . .
. 27
Clothing
130
Cloves, oil of . .
140
Eburnation . .
. 61
Cod-liver oil . .
128
— Cornil and Ranvier on
. 61
Cohnheim
44
— Volkmann on
. 62
Colchicum
138
Ectasine
. 40
Cold, as a cause
21
Effusion, Hoppe - Seyle
r,
Colles
48
analysis of . .
. 56
— on senile arthritis
152
— into joints . .
. 56
Colombel
122
— micro-organisms in
. 56
Conjunctivitis..
123
Electrical bath
. 141
Cornil . . . . 53, 58, 59, 60, 6
— treatment
. 141
— and Ranvier's views on
Emotional causes
. 21
cartilaginous changes
58
Ems
. 148
Corpuscles, granular and
Endocarditis
. 112
amoeboid in diagnosis
56
Endocardium, changes in
.. 66
— nucleated, in blood
67
— micro-organisms on
.. 15
Counter irritants
139
Erb i
56, 141
Creasote . . . . 132,
134
Eucalyptus
.. 139
— action of . .
136
Evans
.. 44
Crepitation in joints. .
101
Eve
.. 4
Crocq
111
Ewing, Dr.
23, 87
Cruveilhier . . . . 3, 6
148
Excision of joints
.. 146
Cysts . .
101
Exostosis
. . 68
— . in connection with senile
Exposure, a cause . .
.. 21
arthritis joints
152
Extension by weights
. . 146
Da Costa
HO
Fagge, Dr. Hilton . . IS
12, 138
Damp
21
Faradism
.. 141
Davies, Lloyd
90
Fats
.. 128
Dax
148
Ferrier, Dr.
38, 39
Deafness
124
— on selective site of musci
dar
Debove, on muscle changes
63
atrophy
.. 39
Deflection of hands
106
Fever
..116
Deformities
105
Fibrous nodules
. . 11 3
— Charcot on. .
107
Fluid in joints
..102
— in gout, chronic rheu-
Foder
23, 87
matism, paralysis agitanp,
Folli
39, 64
etc. . .
111
Forsbrooke, Dr.
8, 26
— types of
107
— views on pathology
.. 26
De Sauvages
4
Franzenbad
.. 143
Desplats
140
Fraxinus excelsior . .
.. 138
'NDEX
169
PAGE
Fuller 3, 7, 88
— on rnorbid anatomy 48, 56
Galvanism . . . . . . 141
Garrod, Sir A, 2, 17, 69, 86, 90
■ — on acute rheumatoid
arthritis . . . . 90
■ — on cardiac lesions . . 112
— on treatment by iodide of
iron
Garrod, Dr. A. E. 8, 17, 18, 30, 43,
49, 56, 70
■ — method of classification 85
— on acute rheumatoid
arthritis . . . . . . 88
— on anaemia of rheu-
matism ...
■ — on cardiac lesions
— on electrical treatment .
— on Heberden's nodes
— on the morbid anatomy .
• — on synovial effusion
— statistics
Gastein
Geist
Germicidal power of blood .
Glands, changes in . .
■ — symptoms due to. .
Gley
Glossy skin
Golgi
Gonorrhoea, a cause . .
Goodhart, Dr.
Gout, a cause. .
— diagnosis of
. — rheumatic
Goutte asthenique primitif
Gowers..
Griffiths, Dr
Guaiacoi
— applied externally
Guaiacols, the
Guaiacoi carbonate . .
nature of and
of administration . ,
. 43
. 112
. 142
. 70
. 48
. 56
. 16
. 148
. 152
. 23
. 67
. 113
. 4U
. 121
. 37
14, 22
. 57
. 22
. 94
3
3
. 116
. 8
. 134
. 140
. 132
. 132
mode
Guaiacum
Gwilt . .
Gymnastics
Habershon
Hadden
Hseniogenesis
Haemogoblin
Haemolysis
135
139
62
130
45
122
42
67
42
PAGE
Hemolytic value of the red
corpuscles . . . . 41, 43
Haemoptysis . . . . . . 119
Haemorrhages.. .. .. 119
Haller 4
Hammam Mes Koutin . . 143
Hammam R'Hira . . . , 143
Hand, deformities of . . . . 106
Harrogate . . . . . . 142
Hay garth . . .. 3, 6, 7, 103
Heart, changes in . . 66
Heberden . . . . 3, 5, 7, 16
— views of the disease . . 5
Heberden's nodes . . 67
Henoch 90
Heredity . . . . 15
Herringham . . . . . 107
Hips, deformities of . . . . 108
— senile arthritis of . . .. 152
Hoelscher . . . . . . 133
Holland, prevalence of the
disease in . .
Homolle . . . . 7,
Hoppe-Seyler . .
Howard
Hudeod
Hunter, Dr. . . . . 41,
— on blood destruction
Husse
Hutchinson . . . . 8,
Hyoscyamus
Haemoly tic process in anaemia 42
Ichthyol
Influenza
Injury
— a cause
Integumentary system, ab-
normalities of . . . . 122
Intermedio-lateral tract . . 40
Iodides.. 138
Iodine 138
— external application of . . 139
Ireland, prevalence of the
disease in . . . . 21
Iritis ..123
Iron 137
Jaccoud . . . . 88, 106
Jenkinson . . . . . . 138
Joints, appearances of 99
— changes in . . . . . . 50
— distension of . . 50
— effusion into . . 56
— haemorrhage into . . 57
— suppuration in . . . . 57
56,
21
98
. 56
. 138
. 133
42, 45
. 42
. 62
25,86
. 139
. 139
. 41
. 6
22
170
IND
EX.
PAGF.
PAGE
Joints, swelling of
99
Monarticu'ar Rheumatoid
— temperature of
100
Arthritis . . . . . . 151
— treatment of
126
Money 90
by excision
146
— on excess of uric acid . . 123
Monocoro . . . . . . 90
Kidney, changes in . .
66
Mont D'or 143
Kissingen
143
Moore, Dr. Norman .. .. 4
Klippel
65
Morbid Anatomy . . . . 48
Knees, deformities of
109
Garrod on . . . . 48
Kohts
21
— — of the bones . . 60
Kolliker
53
— — — — cartilage . . 57
Kussmaul
62
— ligaments . . 50
— synovial mem-
Lacaze-Dori
7, 90
branes . . . . 52
Laker
41
Rindfleisch on . . 48
Lane A.
8
Morbus coxse senilis 85, 151
Lane H.
8
bone marrow in . .
Langen Swalbach
143
Morphia 148
Lanois
140
Motor cells of anterior cor-
Lead, muscular atrophy of .
115
nua of cord . . . . 38, 39
Lebert
4
Folli on 39
Lecethin
56
Moullin Dr. M. . . . . 57
Lecorche
70
Multipolar ganglion cells . . 64
Leis
6
degeneration of . . 64
Leyden
21
Muscles, changes in . . . . 63
Ligaments, changes in
50
— Debove on . . . . . . 63
Linossier
140
— Vallat on 63
Liver, hsemolytic process o
f 42
Muscular Atrophy . . 32, 114
Llangammarch
142
— — an aid to diagnosis . . 94
Lobstein
6
cause of . . . . 115
Local sweatings
40
its extent .. ..37
Loose bodies in joints
53
its nature . . . . 37
Lorain
86
— — neuritis a cause of . . 115
Luchon..
148
reflexes in . . . . 115
Lunn, Dr.
57
result of neuritis . . 116
selected muscles in . . 37
McArdle
85
— — selective character of 114
Mackenzie
41
vaso-motor reflex spasm
Malaria
44
a cause . . . . . . 33
Maltine
129
Musgrave . . . . . . 4
Malum coxee senile . . 6
, 151
Myositis 33
Sandifort on
6
Myotatic irritability . . 120
Mannaberg
44
Meragliano
45
Naked eye appearances of the
Marie
28
joints.. .. .. ..50
Marienbad
20
Naphthols, the . . . . 137
Massage
144
Nephritis 123
Marsolongo
65
Nepven . . . . . . . . 67
Mathieu
7
Nerve arthropathies . . 12
Melon-seed-like bodies
53
Nerve changes . . . . • 92
Mercury
139
— central system, changes in 63
Meyer
6
— inflammatory condition of 29
Micro-organisms, discovery o
f 12
— peripheral, changes in . . 65
found in the joints .
13
— phenomena, early 8, 31
Mitchell
121
— system, symptoms due to 120
INDEX.
171
PAGR
Neumahr . . . . . . 148
Neuritis .. .. ..120
— a cause of muscular
atrophy . . . . . . 115
— as a cause of the disease 28
— descending.. .. ..65
Newsholm Dr. . . . . 43
Nodes, Heberden's . . . . 67
Nodosity of the joints . , 3
Nodules, fibrous . . . . 113
Nomenclature . . . . . . 2
Norse Viking's bones . . 4
Oligochromjemia . . . . 42
Opium . . . . . . . . 140
Ord . . . . 8, 20, 26, 29, 103
Osteitis, rarefying . . . . 62
Osteo-arthritis . . 4, 84, 91
its meaning . . . . 3
Osteoblasts . . . . . . 62
Osteoclasts . . . . 62
Osteophytes . . . . 54
Osteophytic nodules . . . . 100
Osteosclerosis . . . . 62
Osteosclerotic cases . . . . 3
Ostler 41
Paget, Sir James . . . . 32
■ — on glossy skins . . 121
Pain, a symptom . . 101, 105
— its characters . . . . 105
Paraffin . . . . . . 139
Paraldehyde . . . . . . 140
Paralysis agitans . . . . 106
Pathology . . . . . . 25
— Charcot on . . . . 25
— Forsbrooke on . . 26
— Hutchinson on 25
— micro-organisms . . . . 34
— Pye Smith on . . . . 25
— trophic phenomena in . . 37
Periarticular connective tissue 55
Pericarditis . . . . . . 112
Pericardium, changes of . . 66
Pernicious anaemia . . 41, 44
Dr. Hunter on 41, 44
Petrie . . . . . . . . 4
Pfeiffer 70
Phenols, the 136
Phosphates in urine . . . . 123
Phthisis 123
— and Rheumatoid Arthritis 16
Picot 135
Pigmentation, abnormalities
of 40, 122
PAGE
Pitres 29, 65
Pitt Dr. 67
Plombieres 148
Polypi of synovial membrane 53
Post gonorrheal rheumatoid
arthritis . . . . . . 86
Post Gouty Rheumatoid Ar-
thritis " 86
Post Rheumatic Rheumatoid
Arthritis . . . . . . 85
Potassium iodide . . . . 138
Powell, Dr. Douglas . . . . 133
Premonitory symptoms . . 97
Primary spastic paraplegia 32
Primary symptoms . . 97, 99
Prognosis . . . . . . 124
Progressive muscular atrophy 36
Protozoa in malaria
Psoriasis . . . . . . 124
Ptomanies
Puberty 18
Pulmonary Hypertrophic
Osteo Arthropathy . . . . 93
Pulse rate 117
Purpura . . . . . . 119
Pyaemia . . . . 14
Pye-Smith, Dr. . . 17, 25
Pyrogallic acid, action on blood 43
Quinine, the use of . . 136, 138
Rademacker . . . . . . 143
Ranvier . . 53, 58, 59, 60, 61
Reaction of degeneration . . 115
Redfern 7
Reflex action, a cause . . 29
Reflexes in muscular atrophy 115
neuritis . . . . 120
Remak . . . . . . . . 26
Rheumatic Arthritis, Heber-
den's nodes in . . . . 67
Rheumatic gout . . . . 3
■ Fuller on . . . . 7
Rheumatism, a cause . . 23
Rheumatisme articulaire
primitif fixe . . . . 84
generalise . . 85
— chronique primitif . . 3
— fibreux 88
— noueux . . . . 4, 58
Rheumatoid arthritis, acute 87
— — acute rheumatism,
diagnosis from . . . . 93
a constitutional disease 7
— — anaemia in . . . . 118
172
INDEX.
PAGE
Bheumatoid Arthritis, best
term to employ . . . . 1
changes found in the
bones in . . . . . . 4
— — connection with acute
rheumatism . . . . 23
— — deformities in.. .. 105
different from rheuma-
tism, gout, etc., . . . . 7
dislocations in. . .. Ill
due to reflex nerve
impulses . . . . 29
due to simple wear an d
tear . . . . . . . . 8
fever in.. .. .. 116
— — functional depression
a cause . . . . 30
gout, diagnosis from 94
haemorrhages in . . 119
— — Herberden nodes in.. 67
in children . . 90
integumentary system
in ' . . 122
its causes . . 12
its diagnosis . . . . 92
its frequency . . . . 9
— — its meaning . . . . 2
■ its morbid anatomy . . 48
■ its pathology . . 25
its varieties . . 83
micro-organisms in . . 12
■ nature of changes . . 4
nerve symptoms in . . 120
neuritis in . . 29, 120
only a form of chronic
rheumatism . . . . 1
rheumatism, gout and
gonorrhoea, as causes . . 23
— — symptoms of . . . . 97
subacute . . . . 91
tabetic resemblance . . 27
tachycardia in . . 117
toxic products, a cause 31
- — trophic phenomena in 121
— — uterine derangements in 20
vaso-motor disturbances
in 121
various terms applied
to it 3
views held in France 1, 25
Rindfleiscb. . . 48, 57, 58, 59
Rippolsau . . . . . . 143
Rokitansky . . . . 53
Romberg 112
Romerbad . . . . . . 148
PAGE
Sabourin . . . . 33, 37
St. Moritz 143
Salicylates, the use of . . 138
Salol 136
Sand, hot 139
Sandifort . . . . . . 6
Schlauzenbad . . . . . . 148
Schiiller . . . . 79, 86
Scleroderma . . . . 88, 121
Sclerosis of bone . . . . 62
Sclerotitis 123
Scudamore . . . . . . 5
Sea voyage . . . . . . 147
Secondary symptoms . . 97
See 114
Selective action of bacteria
and their products . . 13
— character of muscular
atrophy . . . . 32
Semmola . . ... . . 41
Senator.. .. 8,18,26,56
Senile Arthritis . . . . 157
pathology of . . . . 153
symptoms of . . . . 153
treatment of . . . . 153
Senility, a cause . . 25
Sex ..17
Skin, appearance over joints 99
— changes . . . . 121, 122
Smith, Robert 6
— — on senile arthritis . . 152
Snake poison . . . . . . 44
Spender, Dr 4, 8, 31
on muscular atrophy. . 31
— pigmentation abnor-
malities . . . . . . 31
premonitory symp-
toms 98
taclrycardia . . 31
Spondilitis . . . . . . 105
Steavenson . . . . . . 141
Stimulants, the use of . . 128
Stolzeberg .. .. .. 140
Strathpeffer 142
Striimpell . . . . 33, 37
Subacute Rheumatoid Arthri-
tis 84, 91
its characteristics 91
Sulphonal 180
Sulphur 139
Suppuration In joints 57, 102
Susceptibility . . . . 13
Sweating 122
Sydenham . . . . . . 4
Syers 17
INDEX.
173
PAGK
Symmetry of symptoms . . 104
Symptoms . . . . . . 97
— due to alimentary tract . . 123
— the circulatory sys-
tem .. .. .. ..116
— micro-organisms . . 99
the nerve system . . 120
— premonitory . . . . 97
— primary . . . . 15
— referable to heart . . .. 112
to glands . . . . 113
-to joints . . 99
— secondary . . . . 15, 114
Synovial membrane, thicken-
ing of 99
Syringo-myelia . . 28
Tabes dorsalis . . 27
, 28, 33
Tachycardia
40, 117
Temporo-maxillary joint
.. 103
Tenderness of joints . .
.. 101
Tessier
.. 114
Thermal treatment . .
.. 142
Thumb, deformities of
.. 107
Todd
3, 6, 48
— on cardiac lesions
.. 112
Toluylenediamin
.. 43
Toplitz
.. 143
Toxic products, a cause
.. 31
— albumins
.. 44
Trastour
7, 111
— on deformities
.. Ill
Treatment
.. 126
Trophic changes
.. 28
— phenomena
.. 121
Trousseau . . 4, 17
, 48, 56
— on morbid anatomy
.. 48
Turner, Dr. L.. .
.. 54
Turpentine
.. 139
Urate of Soda deposits
.. 94
Uric acid
7, 123
Urine, changes in
.. 123
Usure des Cartilages Articu-
laire . .
.. 3
page
Uterine derangements, a
cause . . . . . . 20
Vacuolation of nerve cells . . 64
Vaillard 29
Vallat 37, 63
Vapour baths . . . . . . 139
Vaso-motor disturbances . . 121
system . . . . . . 40
action of toxines on 40
Vegetables 128
Vegetations of the synovial
membranes . . . . . . 53
Velvety appearances of the
cartilage . . . . . . 57
Vergely.. .. .. .. 6
Vidal 3, 7, 36
Vierordt . . . . . . 40
Villi of the synovial mem-
brane . . . . 51, 53
Virginia, hot springs of . . 143
Virchow . . . . . . 4, 8
Volkmann . . . . 49, 61, 62
— on osseous changes in
cartilages . . . . . . 60
Vulpian . . . . 32, 38
Wagner 88
Warmbrunn
Weber 6, 59
White corpuscles, increase of 45
Wiesbaden 143
Willbad 143
Wilmot, on senile arthritis . . 152
Wohlmann Dr. A. .. 12,35
Women, frequency of the
disease in . . . . 20
— uterine derangements in . . 20'
Woodhall Spa 142
Wrist, deformities of . . 107
Wynne Dr 60
Zeigler . . . . . . 61
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